ANTIBODY 2
Updated: Sep 9, 2021
ACP's NEW "COVID-19" ANTIBODY GUIDELINES:
Yesterday, the American College of Physicians put out new guidelines in response to "Covid-19" and immunity. What is clear after having read through them is that we are well over a year into this "pandemic" and they know absolutely nothing about the role of antibodies in regards to "Covid-19." These guidelines put a spotlight not only on the antibody scam but the "Coronahoax" as well. A nice overview was presented by Renal and Urology News:
"NEW GUIDANCE: AMERICAN COLLEGE OF PHYSICIANS DISCUSSES ANTIBODY RESPONSE IN COVID-19 IMMUNITY
Because of the novelty of the coronavirus that causes COVID-19, THERE IS NOT ENOUGH EVIDENCE TO DETERMINE WHETHER ANTIBODIES PRODUCED AFTER EXPOSURE ARE PROTECTIVE AGAINST REINFECTION. As such, the American College of Physicians (ACP) published rapid, evidence-based living practice points in the Annals of Internal Medicine discussing the role of antibodies in, tests for diagnosing, and tests for estimating the prevalence of COVID-19.
PRACTICE POINT 1: ANTIBODY TESTS FOR COVID-19 DIAGNOSIS
The ACP DOES NOT RECOMMEND USING SARS-CoV-2 ANTIBODY TESTS to diagnose COVID-19. This recommendation is based on the limited evidence that suggests NOT ALL PATIENTS WITH COVID-19 DEVELOP ANTIBODIES early in the course of their infection, as the PRESENCE AND LEVELS OF ANTIBODIES CAN VARY ACROSS PATIENTS and be dictated by certain disease characteristics.
PRACTICE POINT 2: ANTIBODY TESTS FOR ESTIMATING COMMUNITY PREVALENCE
STUDIES SUGGEST THAT PATIENTS DEVELOP IMMUNE RESPONSES FOLLOWING EXPOSURE TO THE NOVEL CORONAVIRUS. The evidence shows immunoglobulin (Ig)A and IgM antibodies are detectable in the majority of patients who are infected with the SARS-CoV-2 virus. Nearly all patients also demonstrate detectable IgG and neutralizing antibodies.
Over time, THE PREVALENCE AND LEVELS OF THESE ANTIBODIES MAY VARY BY DIFFERENT PATIENT CHARACTERISTICS, DISEASE SYMPTOMS, AND DISEASE SEVERITY. On average, the levels of each of the antibody types peak between 20 to 31 days following symptom onset or polymerase chain reaction diagnosis. Studies also show that the IgM antibodies may persist for up to 115 days and neutralizing antibodies may persist up to 152 days. Therefore, the ACP notes that antibody tests could be feasible options for estimating community prevalence of COVID-19.
PRACTICE POINT 3: THE PROTECTIVE EFFECT OF SARS-CoV-2 ANTIBODIES AGAINST REINFECTION
THERE IS A PAUCITY OF EVIDENCE TO SUGGEST THAT NATURAL IMMUNITY IS CONFERRED BY SARS-CoV-2 ANTIBODIES. THERE IS NO EVIDENCE TO SUGGEST SARS-CoV-2 ANTIBODIES CAN PREDICT THE PRESENCE, LEVEL, OR DURABILITY OF ANY CONFERRED NATURAL IMMUNITY, ESPECIALLY AS IT RELATES TO PROTECTION AGAINST REINFECTION.
Given that most patients exhibit detectable antibodies at least 100 days after infection, IT MAY BE PLAUSIBLE THAT NATURAL IMMUNITY CAN OCCUR. However, the panel reiterates that there is NO DIRECT EVIDENCE TO ANSWER THE QUESTION OF WHETHER THESE ANTIBODIES CAN PROTECT AGAINST REINFECTION.
Some literature indicates that both asymptomatic and symptomatic patients can develop an antibody response indicative of natural immunity following COVID-19, but variables such as disease severity, patient factors, type and amount of antibodies developed, as well as the longevity of those antibodies, play an important role.
The guideline panel cites a small study of hospitalized patients with COVID-19 that reported a single possible case of reinfection during the convalescence stage. This patient did not have IgM or IgG antibodies detected at the 4-week follow-up period.
LIMITATIONS OF THE PRACTICE POINTS
According to the guideline authors, THE PRACTICE POINTS PRESENTED CONCERN ONLY THE ANTIBODY-MEDIATED NATURAL IMMUNITY RESPONSE IN COVID-19 and do not particularly address the involvement of other natural immune responses, including cell-mediated immunity OR VACCINE-ACQUIRED IMMUNITY.
CURRENTLY, THE ONLY EVIDENCE-BASED RECOMMENDATIONS FOR INCREASING IMMUNITY TO THE SARS-CoV-2 VIRUS AND PRESENTING INFECTIONS IS TO RECEIVE AN AUTHORIZED COVID-19 VACCINE. Additional prevention strategies recommended in the guideline include social distancing, wearing a mask in public, quarantining, and regular hand washing.
“GIVEN LIMITED KNOWLEDGE ABOUT THE ASSOCIATION BETWEEN ANTIBODY LEVELS AND NATURAL IMMUNITY,” the guideline authors wrote, “patients with SARS-CoV-2 infection and those with a history of SARS-CoV-2 infection should follow recommended infection prevention and control procedures to slow and reduce the transmission of SARS-CoV-2.”
https://www.renalandurologynews.com/home/departments/mens-health-update/american-college-of-physicians-guidelines-antibody-response-in-sars-cov-2-reinfection
In Summary (Part 1):
-there is NOT ENOUGH EVIDENCE to determine if antibodies produced after exposure provide protection from reinfection
-they recommend not using antibody tests for "Covid-19" diagnosis
-not all patients with "Covid" develop antibodies early
-presence and levels of antibodies vary person to person
-studies SUGGEST patients develop an immune response after "Covid" exposure (except for asymptomatic I suppose...🤷♂️)
-prevalence and levels of antibodies may vary due to patient characteristics, disease symptoms, and disease severity
-there is a PAUCITY (i.e. scarcity) of evidence to suggest that natural antibodies from "Covid" infection confers immunity
-there is NO EVIDENCE to suggest that "Covid" antibodies can predict presence, level, or durability of any conferred immunity, especially regarding reinfection
-they state it MAY BE PLAUSIBLE that natural immunity can occur
-however, they reiterate that there is NO DIRECT EVIDENCE that the antibodies protect against reinfection
-the practice points are only in regards to ANTIBODY-MEDIATED NATURAL IMMUNITY
-they state the only "evidence-based" method to increase immunity is through vaccination (ARTIFICIAL IMMUNITY)
-they admit there is limited knowledge about the association between antibodies and natural immunity
Left out from the Renal and Urology News overview on the ACP's Guidelines were these gems:
"However, LIKE WITH OTHER VIRUSES, THE RELATIONSHIP BETWEEN ANTIBODIES AND NATURAL IMMUNITY MAY VARY ON THE BASIS OF DIFFERENCES IN THE LEVEL AND DURATION OF ANTIBODIES PRODUCED AS WELL AS VIRAL MUTATIONS OF THE INFECTION. When persons are infected with SARS-CoV-2, UNCERTAINTY EXISTS ABOUT WHETHER THE ANTIBODIES PRODUCED (IgM, IgG, IgA, or neutralizing) ARE PROTECTIVE AGAINST REINFECTION, and if so, FOR HOW LONG WHAT LEVELS OF ANTIBODIES ARE NEEDED FOR SUCH PROTECTION (1). In addition, because antibodies to other coronaviruses have been shown to decline over time, how long such protection against reinfection may last also needs to be determined."
"It is also important for clinicians and patients to keep in mind that SARS-CoV-2 antibody test results MAY BE FALSELY POSITIVE DUE TO CROSS-REACTIVITY WITH ANTIBODIES OF OTHER CORONAVIRUSES (74, 75). Furthermore, although a complete assessment of diagnostic accuracy of various antibody tests was beyond the scope of the evidence review, characteristics (for example, SENSITIVITY, SPECIFICITY, AND ACCURACY) VARIED SUBSTANTIALLY AMONG THE ANTIBODY TESTS USED in included studies (3, 4). SUCH VARIATION CAN CONTRIBUTE TO FALSE-NEGATIVE AND FALSE-POSITIVE TEST RESULTS AND ULTIMATELY WRONG CONCLUSIONS (76, 77)."
https://www.acpjournals.org/doi/10.7326/M20-7569
In Summary (Part 2):
-like with other "viruses," the relationship between antibodies and natural immunity MAY VARY
-UNCERTAINTY EXISTS as to whether the antibodies produced (IgM, IgG, IgA, or neutralizing) are PROTECTIVE against reinfection
-they do not know for how long or at what levels these antibodies would be needed for protection
-the antibody tests may produce false-positives due to CROSS-REACTIVITY to other "Coronaviruses"
-test sensitivity, specificity, and accuracy VARIED SUBSTANTIALLY among all of the antibody tests
-the test variation leads to false-negatives, false-positives, and wrong conclusions
So here we are almost a year-and-a-half into this hoax and they have more certainty over the protective effects of the experimental mRNA jab than they do over how the body responds to their "virus" naturally. This is obviously by design. If they can keep people confused/scared about the uncertainty of the protection "natural immunity" does or does not afford, they will be more than happy to line up for the artificial "immunity" of the toxic gene therapy masquerading as a vaccine.
Antibody Testing Is NOT CURRENTLY RECOMMENDED to Assess Immunity After COVID-19 Vaccination:
Did you want more evidence that unproven theoretical antibody measurements are absolutely useless? If so, here you go!
Antibody Testing Is NOT CURRENTLY RECOMMENDED to Assess Immunity After COVID-19 Vaccination: FDA Safety Communication
Date Issued: May 19, 2021
"The U.S. Food and Drug Administration (FDA) is reminding the public and health care providers that RESULTS FROM CURRENTLY AUTHORIZED SARS-CoV-2 ANTIBODY TESTS SHOULD NOT BE USED TO EVALUATE ANY PERSON’S LEVEL OF IMMUNITY OR PROTECTION FROM COVID-19 AT ANY TIME, and especially after the person received a COVID-19 vaccination."
"Recommendations for People Who Had or May Have a SARS-CoV-2 Antibody Test
Be aware that SARS-CoV-2 antibody tests help health care providers identify whether someone has antibodies to SARS-CoV-2, the virus that causes COVID-19, indicating a prior infection with the virus. However, MORE RESEARCH IS NEEDED TO UNDERSTAND THE MEANING OF A POSITIVE OR NEGATIVE ANTIBODY TEST, beyond the presence or absence of antibodies, including in people who received a COVID-19 vaccination, in people who have been exposed and have SARS-CoV-2 antibodies, and in people who are not fully vaccinated.
If you have not been vaccinated: Be aware that A POSITIVE RESULT FROM AN ANTIBODY TEST DOES NOT MEAN YOU HAVE A SPECIFIC AMOUNT OF IMMUNITY OR PROTECTION FROM SARS-CoV-2 INFECTION. If you have a positive test result on a SARS-CoV-2 antibody test, it means that IT IS POSSIBLE you were previously infected with the SARS-CoV-2 virus. Talk with your health care provider about the meaning of your SARS-CoV-2 antibody test results.
If you received a COVID-19 vaccination: Continue to follow the CDC’s recommendations for fully vaccinated people. Be aware that if you have a positive test result on a SARS-CoV-2 antibody test, it is possible you were previously infected with SARS-CoV-2. A COVID-19 VACCINATION MAY ALSO CAUSE A POSITIVE ANTIBODY TEST RESULT FOR SOME BUT NOT ALL ANTIBODY TESTS. YOU SHOULD NOT INTERPRET THE RESULTS OF YOUR SARS-CoV-2 ANTIBODY TEST AS AN INDICATION OF A SPECIFIC LEVEL OF IMMUNITY OR PROTECTION FROM SARS-CoV-2 INFECTION. Talk to your health care provider or your state and local health departments if you have questions about whether an antibody test is right for you.
Recommendations for Health Care Providers
At this time, DO NOT INTERPRET THE RESULTS OF QUALITATIVE, SEMI-QUANTITATIVE, OR QUANTITATIVE SARS-CoV-2 ANTIBODY TESTS AS AN INDICATION OF A SPECIFIC LEVEL OF IMMUNITY OR PROTECTION FROM SARS-CoV-2 INFECTION AFTER THE PERSON HAS RECEIVED A COVID-19 VACCINATION. While a positive antibody test CAN indicate an immune response has occurred (seroconversion), and failure to detect such a response MAY SUGGEST a lack of immune response, MORE RESEARCH IS NEEDED. CURRENTLY AUTHORIZED SARS-CoV-2 ANTIBODY TESTS ARE NOT VALIDATED TO EVALUATE SPECIFIC IMMUNITY OR PROTECTION FROM SARS-CoV-2 INFECTION. SARS-CoV-2 antibody tests should be ordered only by health care providers who are familiar with the use and limitations of the test. For more information about antibody tests for SARS-CoV-2, see Serology/Antibody Tests: FAQs on Testing for SARS-CoV-2.
Be aware that vaccines trigger antibodies to specific viral protein targets. For example, currently authorized COVID-19 mRNA vaccines induce antibodies to the spike protein and not to nucleocapsid proteins that are likely detected only after natural infections. Therefore, COVID-19 vaccinated people who have not had previous natural infection WILL RECEIVE A NEGATIVE ANTIBODY TEST RESULT IF THE ANTIBODY TEST DOES NOT DETECT THE ANTIBODIES INDUCED BY THE COVID-19 VACCINE. If you are considering antibody testing in vaccinated individuals, follow the Centers for Disease Control and Prevention’s guidelines for antibody testing. For more information about antibody test performance visit EUA Authorized Serology Test Performance."
"TEST RESULTS FROM CURRENTLY AUTHORIZED SARS-CoV-2 ANTIBODY TESTS SHOULD NOT BE USED TO EVALUATE ANY PERSON’S LEVEL OF IMMUNITY OR PROTECTION FROM COVID-19. If the results of the antibody test are interpreted as an indication of a specific level of immunity or protection from SARS-CoV-2 infection, there is a potential risk that people may take fewer precautions against SARS-CoV-2 exposure. Taking fewer precautions against SARS-CoV-2 exposure can increase their risk of infection and may result in increased spread of SARS-CoV-2."
https://www.fda.gov/medical-devices/safety-communications/antibody-testing-not-currently-recommended-assess-immunity-after-covid-19-vaccination-fda-safety
In Summary:
-results from currently authorized SARS-CoV-2 antibody tests SHOULD NOT BE USED TO EVALUATE A PERSON’S LEVEL OF IMMUNITY OR PROTECTION FROM COVID-19 AT ANY TIME, and especially after the person received a COVID-19 vaccination
-MORE RESEARCH IS NEEDED TO UNDERSTAND THE MEANING OF A POSITIVE OR NEGATIVE ANTIBODY TEST, beyond the presence or absence of antibodies, including in people who received a COVID-19 vaccination, in people who have been exposed and have SARS-CoV-2 antibodies, and in people who are not fully vaccinated
-a positive result from an antibody test DOES NOT MEAN YOU HAVE A SPECIFIC AMOUNT OF IMMUNITY OR PROTECTION from SARS-CoV-2 infection
-a COVID-19 vaccination may also cause a positive antibody test result FOR SOME BUT NOT ALL ANTIBODY TESTS
-YOU SHOULD NOT INTERPRET THE RESULTS OF YOUR SARS-CoV-2 ANTIBODY TEST as an indication of a specific level of immunity or protection from SARS-CoV-2 infection
-healthcare providers SHOULD NOT INTERPRET THE RESULTS OF QUALITATIVE, SEMI-QUANTITATIVE, OR QUANTITATIVE SARS-CoV-2 ANTIBODY TESTS as an indication of a specific level of immunity or protection from SARS-CoV-2 infection after the person has received a COVID-19 vaccination
-while a positive antibody test CAN indicate an immune response has occurred (seroconversion), and failure to detect such a response MAY SUGGEST a lack of immune response, MORE RESEARCH IS NEEDED
-currently authorized SARS-CoV-2 antibody tests ARE NOT VALIDATED TO EVALUATE SPECIFIC IMMUNITY OR PROTECTION from SARS-CoV-2 infection
-COVID-19 vaccinated people who have not had previous natural infection WILL RECEIVE A NEGATIVE ANTIBODY TEST RESULT if the antibody test does not detect the antibodies induced by the COVID-19 vaccine
-one more time in case they didn't make it clear: Test results from currently authorized SARS-CoV-2 antibody tests SHOULD NOT BE USED TO EVALUATE A PERSON’S LEVEL OF IMMUNITY OR PROTECTION FROM COVID-19
Guess we can put all of this ridiculous antibody nonsense behind us now.
Related Collection on the Antibody Deception:
DO ANTIBODIES EQUAL PROTECTION? THEY DON'T KNOW:
How many antibodies equals protection/immunity? If you are vaccinated but have low or no detectable antibodies, did the vaccine not work? What about if you are vaccinated and still got sick despite high levels of antibodies? If you have too many antibodies, does that mean you have an autoimmune disease due to an overactive immune system? If you have too few antibodies, do you have a weakened immune system?
The answer to all of these questions: THEY DON'T KNOW.
Take, for instance, the amount of antibodies present in a person. Do high or low antibody levels mean protection or rather an overactive or weakened immune system? Maybe...maybe not. It depends:
"If your IMMUNOGLOBULIN LEVEL IS HIGH, it MIGHT be caused by:
Allergies
Chronic infections
An autoimmune disorder that makes your immune system overreact, such as rheumatoid arthritis, lupus, or celiac disease
Liver disease
Inflammatory bowel disease
Cancer, such as multiple myeloma, lymphoma, or leukemia
LOW LEVELS OF IMMUNOGLOBULINS mean your immune system isn't working as well as it should. This can be caused by:
Medicines that weaken your immune system, such as steroids
Diabetes complications
Kidney disease or kidney failure
A weakened immune system that you were born with or developed (as with HIV/AIDS)
JUST BECAUSE YOUR IMMUNOGLOBULIN LEVEL IS HIGH OR LOW DOESN'T MEAN YOU HAVE ONE OF THESE CONDITIONS.
EACH PERSON'S TEST CAN DIFFER based on the method the lab uses to check the results. Talk to your doctor about your test results, and find out what you should do next."
https://www.webmd.com/a-to-z-guides/immunoglobulin-test
THEY DON'T KNOW.
Do antibodies equal protection from Covid-19?
“The risk [for immunocompromised patients] is that you may be operating under the false belief that you’re protected, AND YOU MIGHT NOT BE,” says rheumatologist Jeffrey Curtis, MD, MPH, a Professor of Medicine at the University of Alabama at Birmingham who led the task force that created the ACR COVID-19 Vaccine Clinical Guidance. “BUT IF AN ANTIBODY TEST COMES BACK WITH A CERTAIN NUMBER, NOBODY KNOWS WHAT THAT MEANS.”
In other words, if an antibody test result were to indicate that you had antibodies after the COVID-19 vaccine, THAT DOESN'T MEAN YOU CAN ASSUME YOUR’RE FULLY PROTECTED."
"Experts are still studying the effect of neutralizing antibodies for SARS-CoV-2 in humans. That means your doctor will not be able to tell you what your results mean in terms of your COVID-19 risk, SINCE IT’S NOT YET KNOWN WHAT LEVEL OF NEUTRALIZING ANTIBODIES WOULD BE NEEDED TO PREVENT INFECTION IN YOUR BODY."
"BECAUSE WE DON'T YET KNOW WHAT LEVEL OF ANTIBODIES ARE CORRELATED WITH COVID-19 PROTECTION, neither a “positive” qualitative or “high” quantitative test can tell you for sure if you’re adequately protected or not."
"First of all, NO GUIDE CURRENTLY EXISTS TO TRANSLATE THE RESULTS OF AN ANTIBODY TEST for what it means for your protection from COVID-19.
“At this point, WE DON'T KNOW HOW ANTIBODY PRESENCE OR LEVELS CORRELATE WITH IMMUNITY WELL ENOUGH TO SAY,” says Dr. Ramirez.
"Your antibody level will be a certain number, whether low or high, BUT YOU WON'T KNOW IF THAT’S A LEVEL THAT MEANS YOU’RE ACTUALLY PROTECTED. “NOBODY KNOWS THAT FOR HEALTHY PEOPLE, AND NOBODY KNOWS THAT FOR IMMUNOCOMPROMISED PEOPLE,” adds Dr. Curtis."
“Given the difficulties with interpreting antibody tests, and that we do not yet know if a specific antibody level post-vaccination can predict protection, it would be difficult to make definitive conclusions,” says Dr. Ramirez."
https://creakyjoints.org/living-with-arthritis/coronavirus/covid-19-vaccines/antibody-testing-covid-19-vaccine-immunocompromised
THEY DON'T KNOW.
How do antibody levels relate to protection in regards to other "viruses" and vaccines? Some have high antibody levels, some have low levels. Some are protected, others are not. It depends:
"Antibody levels to different vaccine and virus antigens were measured by their ELISA titer and normalized to the threshold of protection. THE THRESHOLDS FOR PROTECTION WERE TAKEN FROM THE LITERATURE, AND THERE ARE DIFFERENT STANDARDS FOR THE PROTECTION TO DIFFERENT INFECTIONS [26,27]. We calculated the time for antibody titers to fall to the defined threshold for protection for the given vaccine or virus antigen. DUE TO A LACK OF DATA, WE WERE NOT ABLE TO DETERMINE THE CONSEQUENCES OF VARIATION IN THE THRESHOLD FOR PROTECTION BETWEEN INDIVIDUALS. DIFFERENT LEVELS OF IMMUNITY ARE REQUIRED FOR DIFFERENT TYPES OF PROTECTION [27–30]. For example, HIGHER LEVELS of antibodies MIGHT BE REQUIRED TO PREVENT INFECTION, whereas LOWER LEVELS of antibodies MAY NOT PREVENT INFECTION per se BUT MAY STILL AMELIORATE DISEASE or PROTECT AGAINST LETHAL INFECTION."
"We examined the heterogeneity in both the magnitude and decay rate of antibody responses to different virus and vaccine antigens and used simple models to quantify how this heterogeneity affected the duration of protective immunity to a panel of vaccines and viruses. We found that VARIATION IN MAGNITUDE AND DECAY RATES OF RESPONSES CONTRIBUTE COMPARABLY TO THE DIFFERENCES IN ANTIBODY TITERS, that SOME INDIVIDUALS TEND TO MAKE HIGHER RESPONSES and these individuals also tend to have slower decay rates, and that DIFFERENT PATTERNS OF DURATION OF PROTECTIVE LEVELS OF ANTIBODIES WERE ELICITED BY REPLICATING VIRUSES AND PROTEINS."
https://journals.plos.org/plosbiology/article?id=10.1371%2Fjournal.pbio.2006601
THEY DON'T KNOW.
To further illustrate the point that they do not know at what level or even if antibodies provide protection, here is a study on Mumps and antibody "protection" from 2015:
"DYNAMICS OF THE SEROLOGIC RESPONSE IN VACCINATED AND UNVACCINATED MUMPS CASES DURING AN EPIDEMIC"
"ALTHOUGH IT WAS ASSUMED THAT MUMPS VACCINATION INDUCED LIFE-LONG PROTECTION, several mumps outbreaks, ESPECIALLY AMONG VACCINATED STUDENT POPULATIONS, have been reported during the last decade in various countries where mumps vaccination has been implemented into their national immunization programs. In 2009-2012, a mumps epidemic (genotype G) arose that spread across multiple locations within the Netherlands, IN WHICH ALSO PRIMARILY VACCINATED STUDENTS WERE AFFECTED. Waning of vaccine-induced immunity HAS BEEN SUGGESTED to play a role in these outbreaks. When compared to the other components in the MMR vaccine, the mumps component SEEMED TO BE the least effective in eliciting good (high avidity) antibody responses, which were shown to wane to lower levels and in avidity index twenty years after a second MMR vaccination."
"YET OUR UNDERSTANDING OF THE NATURAL SEROLOGIC RESPONSE AGAINST THE MUMPS VIRUS REMAINS INCOMPLETE. Insight is into the ranges in mumps-specific antibody concentrations, their virus-neutralization capacity, as well as in the antibody dynamics seen in time after mumps virus exposure is lacking. The recent epidemic of the Netherlands provided an opportunity to evaluate such aspects of the antibody response following a clinical mumps virus infection."
"The course of anti-mumps IgG and virus-neutralizing (VN) antibody concentrations in 23 clinical mumps cases was investigated, 1-2 months and 7-10 months after onset of disease. SEVEN OF THESE CASES WERE NOT MMR VACCINATED, which made it possible to investigate the difference in the course of antibody response between MMR vaccinated and unvaccinated persons after recent mumps virus infection. In addition, a control group was included in the study, to be able to represent THE LOWER RANGE OF ANTI-MUMPS ANTIBODY LEVELS AS CAN BE EXPECTED IN HEALTHY (non-infected) VACCINES that were age–matched."
"In the Netherlands, a high overall MMR vaccination coverage of 96% and 93% for respectively the first and second dose at 14 months- and 9 years-aged children has been reported. In a large cross-sectional cohort (n=7900) of the Dutch population (2006-2007), it was demonstrated that mumps seroprevalence appeared to be 91%, THEREBY REACHING THE HERD IMMUNITY THRESHOLD OF 86-92% (i.e. threshold percentages of mumps herd immunity combined from two studies, 86–88% and 88–92%). A moderate reduction in seroprevalence, i.e. below or approaching the herd immunity threshold, was observed in several age groups, including the (vaccinated) age group of 15-21 years. THE RELATIVELY LOW MUMPS-SPECIFIC SERUM ANTIBODY LEVELS IN 15-21 YEAR-AGED PERSONS CONFIRMED THE VULNERABILITY OF THIS GROUP WITH RESPECT TO MUMPS VIRUS INFECTION, and may explain the occurrence of the recent epidemic in the Netherlands (2009-2012), five years after this seroprevalence study. This epidemic has been described to count a total of 1,254 laboratory-confirmed mumps cases. THE
MAJORITY OF THE MUMPS CASES was male (59%), university student (47%), 18-25 years of age (68%), and VACCINATED TWICE WITH THE MMR VACCINE (68%). In the present study, two clear response patterns in IgG and VN antibody levels against the mumps vaccine strain could be detected in consecutive blood samples obtained from mumps virus infected persons during this epidemic. In previously vaccinated mumps cases, specific IgG concentrations as well as the ND50 values were significantly
higher shortly (1-2 months) after onset of disease than at 7-10 months. This pattern in antibody response characterizes a secondary response, i.e. rapid production of antibodies upon subsequent encounter with the same antigen. Alternatively, UNVACCINATED MUMPS CASES ALSO MOUNTED A SERORESPONSE, BUT OF GENERALLY LOWER IgG ANTIBODY CONCENTRATIONS AND ND50 VALUES AT BOTH SAMPLING POINTS THAN CASES WHO HAD RECEIVED 2 MMR VACCINE DOSES. The overall IgG concentrations or ND50 values of the unvaccinated cases did not differ significantly between the two time points, and two out of the seven unvaccinated mumps cases had a lower IgG antibody response 1-2 months compared with 7-10 months after onset of disease. This antibody pattern is illustrative of a primary response. It is striking that FOUR OUT OF THE SEVEN UNVACCINATED MUMPS CASES WERE AGED ≥ 40 YEARS, and it is likely, although not certain, that these persons had encountered wild-type mumps virus earlier in life. However, although NATURAL INFECTION WITH MUMPS IS THOUGHT TO CONFER LIFELONG PROTECTION, INCIDENTALLY CASES OF REINFECTIONS HAVE BEEN DESCRIBED, and with the absence of circulating wild-type mumps virus also naturally-acquired immunity against mumps may diminish. In addition, it must be kept in mind that in our assays ANTIBODIES WERE MEASURED AGAINST THE MUMPS VACCINE STRAIN, which may result in a relatively lower response in persons with naturally-acquired immunity induced by other mumps virus strain(s). One of the two persons who showed a rise in mumps-specific IgG antibody level in time, SUGGESTIVE OF A PRIMARY RESPONSE, WAS AGED > 50 YEARS, but the observed virus-neutralizing (VN) antibody response of this particular person was NOT TYPICAL FOR A PRIMARY RESPONSE."
"The study design, i.e. observational study with limited sample size, DID NOT ALLOW DETERMINATION OF WHY MUMPS CASES BECAME INFECTED DESPITE VACCINATION."
"Notwithstanding its limited sample size, our
present study describes how mumps-specific antibody concentrations and their virus-neutralization capacity develop in time after mumps virus infection; the antibody response was significantly higher in the vaccinated mumps cases compared to the unvaccinated cases at both sampling times,
SUGGESTIVE OF A BETTER AND MORE PRONOUNCED IMMUNITY AGAINST MUMPS. Although the humoral response certainly plays a role in protection against mumps, IT SHOULD BE CONSIDERED THAT IN VITRO MEASURED VN ANTIBODY CONCENTRATIONS, BUT ALSO IgG CONCENTRATIONS, MAY NOT BE FULLY PREDICTIVE OF IMMUNOLOGICAL ANTIBODY ACTIVITY IN VIVO, given that Fc-mediated phagocytosis, antibody-dependent cell-mediated cytotoxicity, and other processes that occur in the host are not reflected in the
corresponding assays. Additionally, other immune mechanisms, such as cellular immunity, are likely involved in the protection against mumps disease as well as in the viral clearance. THE CELLULAR IMMUNITY AGAINST MUMPS HAS ONLY BEEN SCARCELY EXPLORED AND DESERVES MORE ATTENTION."
"Summarizing, mumps patients developed high levels of both mumps-specific IgG
concentrations and mumps VN antibodies; vaccinated patients had higher antibody levels than unvaccinated patients. Antibody dynamics of vaccinated versus unvaccinated mumps cases differed, i.e. vaccinated mumps cases had higher antibody levels 1-2 months after onset of disease that declined at 7-10 months, which is characteristic of a secondary response. PREVIOUS MMR VACCINATION RESULTED IN HIGHER (functional) ANTIBODY LEVELS IN THE MUMPS CASES, probably by pre-existing B cell
memory, ALTHOUGH IT WAS NOT EFFECTIVE ENOUGH TO PREVENT MUMPS VIRUS INFECTION."
"Seven out of the 23 mumps cases were unvaccinated and 16 CASES WERE PREVIOUSLY VACCINATED WITH TWO DOSES OF THE MMR VACCINE. In addition, 20 healthy control persons (25 yrs (22-29 yrs; 35% male) were included who had no symptoms of mumps or evidence of recent mumps virus infection based on serologic data. Two out of the 20 healthy controls (aged 55 and 57 years) were unvaccinated, and 18 CONTROLS WERE PREVIOUSLY VACCINATED WITH TWO DOSES OF THE MMR VACCINE."
"MUMPS-SPECIFIC IgG CONCENTRATIONS WERE ANALYZED USING THE MUMPS VACCINE STRAIN (Jeryl Lynn (JL)) AS ANTIGEN. The fluorescent bead-based multiplex immunoassay (MIA) using Luminex technology was performed as described before. Briefly, plasma samples were diluted 1/200 and 1/4,000 in phosphate buffered saline containing 0.1% TWEEN 20 AND 3% BOVINE SERUM ALBUMIN."
Mumps virus-neutralizing (VN) antibodies were detected by focus reduction neutralization
test (FRNT), partly based on the protocol described by Vaidya et al.34 Mumps vaccine virus (JL strain; stored at -80°C) was thawed and mixed with heat-inactivated (45 min 56°C) plasma samples (both 37.5 µl) to be incubated for 2 hours at 37°C. CULTURE MEDIUM (DULBECCO’S MODIFIED EAGLE MEDIUM
(Life Technologies) SUPPLEMENTED WITH 5% FETAL CALF SERUM, PENICILLIN, STREPTOMYCIN, and L-glutamine) WAS REMOVED FROM VERO CELLS (2 x 104 cells/mL) AND 50 µl OF VIRUS/PLASMA MIXTURE WAS ADDED TO EACH WELL of a 96 wells plate (i.e. > 20 plaques mumps virus per well). Plates were incubated for 4 hours at
36°C, wells were emptied and 200 µl of 0.8% carboxymethylcellulose medium was added to each well. Plates were incubated for 40 hours at 36°C with 5% CO2, before they were washed with PBS and subsequently fixed with a mixture of aceton and methanol (2:3). After 10 min, plates were washed with ice-cold PBS, and incubated with block buffer (PBS containing 1% BSA) for 30 min at 36°C. ANTI-MUMPS NUCLEOPROTEIN ANTIBODY (Abcam) WAS IN BLOCK BUFFER (1:3000) AND 100 µl WAS ADDED TO EACH WELL. After incubation for 1 hour at 36°C, plates were washed with PBS CONTAINING 0.1% TWEEN-20 (PBST). Subsequently, 100 µl OF GOAT-ANTI-MOUSE IgG-HRP (DAKO) IN BLOCK BUFFER (1:2000) WAS ADDED TO EACH WELL and plates were incubated for one hour at 36°C. Plates were washed with PBST and wells were stained with 50 µl of TrueBlue peroxidase substrate (KPL, Inc.). The numbers of plaques were counted and the 50% VN antibody dose (ND50) of each sample was calculated. The WHO international standard RubI-1-94 (NIBSC) was used as positive control in each assay run and to calculate relative ND50 value IN ORDER TO ADJUST FOR INTER-ASSAY DIFFERENCES.``
doi: 10.1080/21645515.2015.1040967
In Summary:
-it was ASSUMED mumps vaccination led to life-long immunity
-this assumption has been challenged by several mumps outbreaks in highly vaccinated populations among those who have received 2 doses of the MMR vaccine
-vaccinated students were primarily affected
-they presume waning vaccine-induced immunity/antibody levels are at fault
-the mumps component of the MMR seemed to be the least effective at eliciting high antibody response
-they admit that the knowledge of the serologic response to mumps remains incomplete
-they looked at 23 mumps cases, 7 of which were not vaccinated with MMR while the rest were
-a "control" group of healthy vaccinated individuals were included to show low-level antibody protection
-the Dutch population had reached the 91% vaccination threshold for "herd immunity" yet were still experiencing outbreaks among the vaccinated
-low levels of antibodies in the 15-21 year-old age group meant they were vulnerable even with the "herd immunity" threshold achieved
-the majority (68%) of the mumps cases were among those vaccinated with the MMR vaccine 2x
-vaccinated mumps cases had higher antibody levels than the unvaccinated
-4 of the 7 unvaccinated mumps cases were above 40 years of age which SUGGESTED they encountered mumps earlier in life
-while natural infection with mumps is supposed to confer lifelong immunity, they admit reinfections do occur
-antibodies in this study were measured against the VACCINE strain
-an over 50 unvaccinated individual had a IgG response suggestive of a primary response but the neutralizing antibody response was not suggestive of a primary response
-the limited sample size did not allow for them to determine why mumps cases occurred in the vaccinated
-the higher antibody response in the vaccinated mumps cases were SUGGESTIVE of a better immune response than the unvaccinated group -however, they admit that results from experiments done IN VITRO (outside the body) do not necessarily equate to what actually occurs immunologically IN VIVO (in the body)
-they admit cellular immunity against mumps is scarcely explored and needs further research
-they conclude that previous MMR vaccination resulted in higher antibody levels but this did not offer protection against mumps
In other words: THEY DON'T KNOW.
ANTIBODY MADNESS! MISSING ANTIBODY, MISSING PROTECTION?:
SEROCONVERSION: The development of detectable antibodies in the blood that are directed against an infectious agent.
https://www.medicinenet.com/seroconversion/definition.htm
On April 20th, 2021 a study was published which attempted to look at the antibody response in regards to influenza infection. They were trying to decipher why some people mount a strong antibody response while others do not. Within the study is a great deal of information on the lack of seroconversion (detectable antibodies) in many cases of disease.
Unfortunately for the researchers, instead of uncovering why this lack of seroconversion occurs, their results showed that airway monocytes, which are typically associated with severe disease, were somehow linked to a protective effect. Obviously wanting to have their cake and eat it too, they concluded that sometimes immune factors play a protective role and other times they play a pathogenic role:
“THE IMMUNE FACTORS THAT EXPLAIN WHY SOME PEOPLE MOUNT A STRONG ANTIBODY RESPONSE AND OTHERS DON'T HAS NOT BEEN WELL UNDERSTOOD,” said Richard Webby, PhD, of the Infectious Diseases Department. “This study identifies some of those factors, providing information needed to design more effective vaccines for flu and other viruses.”
“Airway monocytes often show up AS CORRELATES OF SEVERE DISEASE, so it was interesting here to see them also associated with PROTECTIVE IMMUNE RESPONSES,” said Paul Thomas, PhD, of the Immunology Department. “IT POINTS TO THE FACT THAT MANY IMMUNE FACTORS PLAY PROTECTIVE AND PATHOGENIC ROLES AT THE SAME TIME.”
https://blogs.stjude.org/progress/flu-clues-antibody-production-immune-markers
While their conclusion regarding the simultaneous opposing nature of immune system factors is absolutely absurd, this study had some very insightful admittances along with some great links to other relevant research. Below are highlights from the 2021 study followed by a few quick highlights from some of the related studies:
ACTIVATED CD4+ T CELLS AND CD14hiCD16+ MONOCYTES CORRELATE WITH ANTIBODY RESPONSE FOLLOWING INFLUENZA VIRUS INFECTIONS IN HUMANS
"THE FAILURE TO MOUNT AN ANTIBODY RESPONSE following viral infection or seroconversion failure IS A LARGELY UNDERAPPRECIATED AND POORLY UNDERSTOOD PHENOMENON."
"INTRODUCTION
AN INCREASE IN ANTIGEN-SPECIFIC ANTIBODY TITER IN THE SERUM, known as seroconversion, HAS LONG BEEN ACCEPTED TO BE A SEROLOGICAL HALLMARK OF A RECENT INFECTION OR ANTIGEN EXPOSURE. However, the advent of molecular diagnosis has led to the observation that SOME INFECTIONS DO NOT ALWAYS RESULT IN THE SUBSEQUENT PRODUCTION OF DETECTABLE ANTIBODIES, PARTICULARLY THOSE WITH NEUTRALIZING AND PROTECTIVE ACTIVITY. This has been documented in infections with INFLUENZA virus,1, 2, 3, 4, 5 HUMAN CORONAVIRUSES,6 the MIDDLE EAST RESPIRATORY SYNDROME (MERS) coronavirus, 7 and the recently emerged SEVERE ACUTE RESPIRATORY SYNDROME-CORONAVIRUS-2 (SARS-CoV-2)8,9 infections. THE IMMUNOLOGICAL MECHANISMS UNDERLYING SEROCONVERSION FAILURE ARE NOT WELL UNDERSTOOD, but a better understanding is important, particularly for vaccine design."
"In humans, THE MAJORITY OF OUR UNDERSTANDING OF WHAT IS REQUIRED FOR THE GENERATION OF A ROBUST ANTIBODY RESPONSE HAVE BEEN DERIVED FROM VACCINATION STUDIES. Such studies have the advantage of having temporally defined pre- and post-antigen exposures that facilitate sample and data acquisition and have used targeted or systems-wide approaches to identify correlates of robust antibody production."
"However, given the differences in antigenic composition and exposure route, POST-VACCINATION RESPONSES MAY NOT NECESSARILY REFLECT THE POST-INFECTION IMMUNE RESPONSE, particularly for respiratory viral infections."
"For influenza viruses, antibodies that target the major surface viral glycoproteins, hemagglutinin (HA) and neuraminidase (NA) are induced after infection. In terms of sero responses to influenza virus infection, HA antibodies measured in a HEMAGGLUTINATION-INHIBITION (HAI) ASSAY ARE CONSIDERED TO BE THE GOLD STANDARD. Antibodies detected by HAI assay primarily bind to the HA globular head, which contains the receptor-binding domain and the major antigenic sites. These antibodies confer high antigenic specificity and can provide potent protection from infection in humans and animal studies.21,22 THE HAI ASSAY DOES NOT STRICTLY MEASURE VIRUS NEUTRALIZING ACTIVITY, but its relative ease of use and ESTABLISHED CORRELATION WITH PROTECTION 21, 22, 23 have justified its use as a major serological endpoint in influenza vaccine and infection studies. SERUM HAI-ANTIBODY TITERS ≥40 HAVE BEEN SHOWN TO BE ASSOCIATED WITH PROTECTION FROM SEASONAL INFLUENZA VIRUS INFECTIONS 21 AND HAVE BEEN ADOPTED AS THE MINIMAL IMMUNOGENICITY REQUIREMENT for the licensure of seasonal influenza vaccines.24 Compared to HA, NA ANTIBODIES ARE LESS WELL STUDIED, although they have also been recently identified as a potential additional correlate of protection from severe influenza disease."
"THE FAILURE TO SEROCONVERT BY THE STANDARD HAI ASSAY AFTER LABORATORY-CONFIRMED INFLUENZA VIRUS INFECTION HAS BEEN REPORTED IN SEROEPIDEMIOLOGICAL,1,2 VACCINATION,27 AND EVEN CHALLENGE STUDIES.3, 4, 5,28 A review of human challenge studies showed that BETWEEN 50% AND 90% OF INDIVIDUALS WITH PCR CONFIRMATION OF INFLUENZA VIRUS INFECTION FAILED TO SEROCONVERT by HAI assay.3, 4, 5,28 THE UNDERLYING IMMUNOLOGIC FACTORS DRIVING THE MAGNITUDE OF THE ANTIBODY RESPONSE FOLLOWING INFLUENZA VIRUS INFECTION IS STILL, however, POORLY DEFINED."
"In the SHIVERS cohort, participants were enrolled according to the World Health Organization (WHO) case definition for influenza-like illness (ILI) or severe acute respiratory illness (SARI) from general practices or hospitals in Auckland between August and October 2013, which coincided with the peak influenza season in New Zealand.29 Of those with PCR-confirmed infection (N = 66), 21 (32%) PARTICIPANTS MET THE DEFINITION OF HAI SEROCONVERSION (at least a 4-fold increase in antibody titer in the paired sera)."
"Having determined the correlations between CD16+ monocytes and serum antibody responses, we next asked whether similar patterns were seen in the mucosal compartment. To address this, we measured the influenza-specific IgA and IgG titers in the nasal washes of influenza-confirmed individuals from a cohort in which we had previously characterized their monocyte subpopulations.31 AS THERE IS NO EQUIVALENT SEROCONVERSION STANDARD FOR MUCOSAL ANTIBODY TITERS, we identified 10 individuals with influenza-specific IgA titer >40 in their nasal wash samples within 2 weeks of symptom onset as SCs (GMT, 95% CI: 186.6, 98.4–354.1) (Figure 4A) AND ANOTHER 9 INDIVIDUALS, WITH NO DETECTABLE IgA TIGERS DURING THE COURSE OF STUDY, as non-SCs (Table S2). To ensure the validity of our classification of SCs and non-SCs, we also evaluated the influenza-specific IgG responses. Nine of the 10 SCs had influenza-specific IgG titers >40 (GMT, 95% CI: 28.9, 2.8–292), WHILE NONE OF THE NON-SCS HAD DETECTABLE TITERS AT ANY OF THE TIME POINTS TESTED (Figure 4B)."
"DISCUSSION
Seroconversion in influenza is typically defined by measuring the strain-specific HAI antibody response and is GENERALLY THOUGHT TO FOLLOW INFECTION. Somewhat unexpectedly, WE FOUND THAT ONLY 32% OF INDIVIDUALS WHO WERE PCR CONFIRMED TO BE INFECTED WITH INFLUENZA VIRUS MET THIS STANDARD DEFINITION OF SEROCONVERSION in SHIVERS."
"THE HIGHER INCIDENCE OF SEROCONVERSION IN HOSPITALIZED INDIVIDUALS SUPPORTS A CORRELATION BETWEEN THE SEVERITY OF INFECTION AND ANTIBODY RESPONSIVENESS in the periphery and nasal mucosa.5,41 Although our data cannot preclude the possibility of antibody-dependent enhancement (ADE) of influenza disease, we think it is unlikely within the context of our study design (antibody increases were detected post-hospitalization) and other available evidence. ADE of influenza disease has mostly been described during the 2009 H1N1 pandemic 42,43 and within critically ill or fatal cases.44,45 In our cohort, although they were hospitalized, most of the patients were on the “milder” end of the severity spectrum.36 Furthermore, in the present and previous SHIVERS studies on the immunological correlates of disease severity, WE FOUND NO SIGNIFICANT DIFFERENCES IN THE ACUTE-PHASE ANTIBODY TITERS BETWEEN MILD (outpatient) AND SEVERE (hospitalized) PATIENTS. Thus, it appears that, paradoxically, A STRONG PROINFLAMMATORY RESPONSE THAT IS ASSOCIATED WITH SYMPTOMATIC INFECTIONS 31,36 COULD ALSO HELP INDUCE A GOOD ANTIBODY RESPONSE, WHILE A WEAK SIGNAL MAY NOT PROVIDE ADEQUATE STIMULATION.46 This is a particularly important consideration for the ongoing coronavirus disease 2019 (COVID-19) pandemic, in which A PROPORTION OF MILD OR ASYMPTOMATIC COVID-19 CASES FAIL TO MOUNT DETECTABLE ANTIBODY RESPONSES DESPITE EVIDENCE OF ACTIVE INFECTION, WHILE SEVERELY ILL PATIENTS HAD COMPARABLY STRONGER ANTIBODY RESPONSES.8,9,47 Incidentally, the lack of association between age and seroconversion indicates that disease severity may be a stronger factor driving post-infection antibody response than age, suggesting a strong proinflammatory response may compensate for the decline in immune function in the elderly. However, it should be noted that THE ASSOCIATION BETWEEN ANTIBODY RESPONSE AND SEVERITY OF INFECTION SHOULD NOT BE BROADLY INTERPRETED, AS IT HAD ALSO BEEN SHOWN THAT FATAL H7N9 AND COVID-19 PATIENTS FAILED TO MOUNT ROBUST ANTIBODY RESPONSES IN SOME CASES.47,48
"In summary, our data provide immunological evidence that RESPIRATORY VIRAL INFECTIONS DO NOT ALWAYS LEAD TO SUCCESSFUL SEROCONVERSIONS. These data have implications for our understanding of post-infection immunity and on studies that rely on such metrics."
"Finally, IT IS UNKNOWN WHETHER THE PRESENT FAILURE TO MOUNT AN ANTIBODY RESPONSE WOULD HAVE ANY IMPACT ON THE MEMORY B CELL RESPONSES and their capacity to mount a recall response."
https://www.sciencedirect.com/science/article/pii/S2666379121000537
In Summary (Part 1):
-the failure to mount an antibody response is an underappreciated and poorly understood phenomenon
-an increase in antibody titer in the serum has long been the hallmark of evidence for a recent infection or antigen exposure
-however, it has been observed that not all infections result in detectable antibody production, particularly those with neutralizing and protective activity
-this lack of antibodies has been repeatedly observed in influenza, human coronaviruses, MERS, and SARS-COV-2 cases
-the immunological mechanism for antibody failure is not well understood
-the majority of the understanding on what is required to get a robust antibody response comes from vaccination studies
-post-vaccination antibody responses may not reflect post-infection antibody responses
-hemagglutination-inhibition (HAI) assay is considered the gold standard for measuring antibody activity
-HAI does not strictly measure "virus" neutralizing antibody activity yet it is CORRELATED with protection
-serum antibody titers >40 are associated with protection and are the minimal immunogenicity requirement for vaccines
-NA antibodies are less well studied
-failure to seroconvert has been shown in seroepidemiological, vaccination, and challenge studies
-between 50 to 90% of PCR CONFIRMED influenza cases failed to seroconvert
-the underlying immunologic factors driving the magnitude of the antibody response following influenza infection is still poorly defined
-only 32% (21 of 66) of participants in the study met the seroconversion definition
-there is no seroconversion standard for mucosal antibody titers
-9 individuals had no detectable IgA levels
-9 of 10 seroconverters had detectable IgG while none of the non-seroconverters ever had detectable IgG
-seroconversion is generally thought to occur after infection
-they reiterate that only 32% of the participants seroconverted with detectable antibody levels in their study
-they state that a higher rate of seroconversion in hospitalized patients CORRELATES with severity of disease and increased antibody levels
-they found no differences in antibody levels of those with mild or severe illness
-they think a strong proinflammatory response may lead to greater antibody production over a weaker response
-with "Covid-19," mild and asymptomatic cases had no antibody response while those with severe illness had higher levels
-however, they state that the association between disease severity and antibody production should not be broadly interpreted as there were fatal H7N9 and "Covid-19" cases which also failed to mount antibody responses
-they conclude that respiratory "viruses" do not always lead to antibody production
-they do not know whether the failure to mount an antibody response has any impact on B cell response
Here is a quick roundup of highlights from a few of the linked studies stating infections do not always result in detectable antibodies:
"Appropriately timed paired serology detects 80-90% RT-PCR confirmed H1N1-2009; ANTIBODIES FROM INFECTION WITH H1N1-2009 CROSS-REACTED WITH SEASONAL INFLUENZA VIRUSES."
https://pubmed.ncbi.nlm.nih.gov/20814575/
"Conclusion: Following the June-September 2009 wave of 2009 influenza A(H1N1), 13% OF THE COMMUNITY PARTICIPANTS SEROCONVERTED, and most of the adult population likely remained susceptible."
https://pubmed.ncbi.nlm.nih.gov/20388894/
"Although NO CORRELATION BETWEEN THE INFLUENZA VIRUS–SPECIFIC B-cell RESPONSE AND SEROLOGICAL HI ANTIBODY LEVEL WAS FOUND, these data clearly supported that acute infections could quickly induce the recalling response of virus-specific B cells, EVEN WHERE THE PREEXISTING ANTIBODY LEVEL IS UNDETECTABLE."
https://academic.oup.com/jid/article/209/9/1354/886344
"THIS STUDY REPRESENTS THE FIRST TIME THE CURRENT GOLD STANDARD for evaluating influenza vaccines as set by the U.S. Food and Drug Administration and the European Medicines Agency Committee for Medicinal Products for Human Use, A "PROTECTIVE" hemagglutination inhibition (HAI) titer of ≥1:40, HAS BEEN EVALUATED IN A WELL-CONTROLLED HEALTHY VOLUNTEERS CHALLENGE STUDY SINCE THE CUTOFF WAS ESTABLISHED. We used our established wild-type influenza A healthy volunteer human challenge model to evaluate how well this antibody titer predicts a reduction in influenza virus-induced disease. We demonstrate that although higher HAI titer is predictive of some protection, there is stronger evidence to suggest that neuraminidase inhibition (NAI) titer is more predictive of protection and reduced disease."
"The U.S. Food and Drug Administration and the European Medicines Agency Committee for Medicinal Products for Human Use both define “protective” titers as a hemagglutination inhibition (HAI) titer of ≥1:40 (7).
THE EVIDENCE FOR THIS CUTOFF COMES FROM A SEMINAL LIVE INFLUENZA VIRUS CHALLENGE TRIAL CONDUCTED IN 1972 by Hobson et al., which established that a pre challenge serum HAI titer of 18 to 36 was ASSOCIATED WITH 50% PROTECTION from infection (and a similar study demonstrating a 29% infection rate in those with HAI titers of 1:40 to 60 (9). OTHER STUDIES IN THE SETTING OF LIVE AND ATTENUATED INFLUENZA VIRUS CHALLENGE HAVE BEEN LESS CONCLUSIVE (10,–12). A more recent study, conducted using live attenuated viruses, demonstrated 50% protection from intranasal infection in those with titers of ≥1:40 (13), BUT A RECENT EPIDEMIOLOGICAL STUDY OF VACCINES PERFORMANCE HAS BROUGHT THIS INTO QUESTION, WITH ONLY 22% PROTECTION OF CHILDREN WITH POST VACCINATION TITERS OF ≥1:40 (14). Even more concerning are data from the recent influenza seasons suggesting that CURRENT SEASONAL VACCINES HELD TO THESE STANDARDS ARE GREATLY UNDERPERFORMING, as overall seasonal vaccine effectiveness over the past 10 years HAS RANGED FROM 10 TO 56% WITH A MEAN OF 40% (15)."
"ANTIBODY RESPONSES WERE MEASURED POSTCHALLENGE DEMONSTRATING NO SIGNIFICANT INCREASE IN THE HAI GMT IN THE HIGH-HAI-TITER GROUP after challenge (week 😎, but a clear increase was noted in the low-HAI-titer group (Fig. 7A). THE RESPONSE IN THE LOW-TITER GROUP WAS VARIABLE, WITH APPROXIMATELY 50% OF THOSE PARTICIPANTS SHOWING A VERY SIGNIFICANT >4-FOLD RISE IN TITER, WHILE THE OTHER 50% OF PARTICIPANTS SHOWED NO SIGNIFICANT INCREASE IN HAI TITER (Fig. 7B)."
"IF THESE RESULTS ARE CONSISTENT WITH OUTCOMES FOLLOWING NATURAL INFLUENZA INFECTION, THE PROTECTION AFFORDED by an HAI titer of ≥1:40 WOULD NOT NECESSARILY INCLUDE THE PREVENTION OF A CLINICAL INFLUENZA-LIKE ILLNESS"
"APPROXIMATELY 50% OF THOSE WITH LOW BASELINE HAI TITERS HAD NO SIGNIFICANT RISE IN TITER. Those who demonstrated no rise in titer were JUST AS LIKELY TO DEVELOP MMID AND THE SEVERITY OF DISEASE OF THESE INDIVIDUALS WAS SIMILAR TO THOSE WHO DID RESPOND, ruling out the possibility of no infection in these cases."
"ALTHOUGH A CHALLENGE STUDY OF THIS TYPE DOES NOT NECESSARILY REPLICATE HOW HUMANS BECOME INFECTED WITH INFLUENZA NATURALLY, it still points out the importance of careful consideration of how protection is defined and suggests a strategy by which evaluation of the correlates of protection to influenza can lead to improved evaluation of vaccine efficacy."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4959521
"NO EVIDENCE FOR TRANSMISSION OF the ca or ts-1A2 recombinant VIRUS TO CONTROLS WAS OBSERVED. A SERUM hemagglutination inhibition RESPONSE WAS DETECTED IN LESS THAN 50% OF THE INFECTED VACCINES."
https://pubmed.ncbi.nlm.nih.gov/7216417/
"We evaluated serologic response of 42 Middle East respiratory syndrome coronavirus (MERS-CoV)-infected patients according to 4 severity groups: asymptomatic infection (Group 0), symptomatic infection without pneumonia (Group 1), pneumonia without respiratory failure (Group 2), and pneumonia progressing to respiratory failure (Group 3). NONE OF THE GROUP 0 PATIENTS SHOWED SEROCONVERSION, while the seroconversion rate gradually increased with increasing disease severity (0.0%, 60.0%, 93.8%, and 100% in Group 0, 1, 2, 3, respectively; P = 0.001). Group 3 patients showed delayed increment of antibody titers during the fourth week, while Group 2 patients showed robust increment of antibody titer during the third week. AMONG PATIENTS HAVING PNEUMONIA, 75% OF DECEASED PATIENTS DID NOT SHOW SEROCONVERSION BY THE THIRD WEEK, while 100% of the survived patients were seroconverted (P = 0.003)."
https://pubmed.ncbi.nlm.nih.gov/28821364/
"For the eight patients in the asymptomatic/mild symptom group, NONE HAD POSITIVE anti-SARS-CoV-2 IgM RESULTS AND THREE (cases 11-13) HAD NEGATIVE anti-SARS-CoV-2 IgG RESULTS (Fig. 1B)."
"Several limitations were found in our study. First, the sample size is small, as we included only 14 COVID-19 patients. Second, A FURTHER WESTERN BLOT ASSAY for detecting the anti-SARS-CoV-2-specific protein IgG or IgM antibodies WAS NOT PERFORMED TO VALIDATE THE PERFORMANCE of the ALLTEST 2019-nCoV IgG/IgM Rapid Test AND UNDERSTAND THE INCONSISTENCY IN THE PRESENCE OF anti-SARS-CoV-2 IgM AND IgG. Third, CROSS REACTION OF SERUM SPECIMENS from the acute phase of different viral infections (e.g., influenza, respiratory syncytial virus, and rhinovirus.) in the IgM portion of this SARS-CoV-2 assay WAS NOT PERFORMED."
"Patients with symptoms and development of anti-SARS-CoV-2 IgM antibodies had a shorter duration of positive rRT-PCR result and no worsening clinical conditions COMPARED TO THOSE WITHOUT THE PRESENCE OF anti-SARS-CoV-2 IgM ANTIBODIES."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7177139
"Serological antibody tests were performed at different times post–disease onset. The overall antibody positivity was 93.75% (105/112). Fifty-eight of 112 patients (51.79%) were positive for IgM (20.93 ± 45.94 AU/mL, mean ± SD) and IgG (122.26 ± 60.94 AU/mL), 7 (6.25%) WERE NEGATIVE FOR BOTH ANTIBODIES, 1 (0.89%) WAS POSITIVE FOR IgM WITH NO RESPONSE TO IgG, AND 46 (41.07%) WERE POSITIVE FOR IgG BUT NOT FOR IgM."
https://academic.oup.com/jid/article/222/2/183/5828055
In Summary (Part 2):
-antibodies from H1N1 cross-reacted with those of seasonal influenza "virus" (i.e. they were NOT SPECIFIC)
-only 13% of H1N1 patients seroconverted (i.e. had detectable antibodies)
-no correlation between B cell and HI antibody levels were found yet it was concluded that even in the absence of antibodies, B cell recall occurred
-the gold standard "PROTECTIVE" HAI of >40 was evaluated by human challenge trials
-the HAI >40 cutoff was established off of one study in 1972 with results only showing 50% were protected
-more recent studies have challenged the HAI cutoff
-one study found only 22% of children with HAI > 40 were "protected" after vaccination
-seasonal vaccines held to this standard consistently fail and fall anywhere from 10% to 56% in effectiveness with a mean of 40%
-postchallenge, there was no increase in antibody levels in the high HAI group
-postchallenge, only 50% of the low HAI group saw an increase in antibody levels while the other 50% saw none
-if the challenge results are consistent with real world infections, the HAI of >40 would NOT PREVENT clinical Influenza-like illness
-those with low HAI were just as likely to develop mild moderate Influenza disease and the severity to those with high HAI levels was comparable
-the challenge trials do not replicate how humans are infected naturally
-no evidence of transmission of recombinant "virus" to controls was observed
-an HAI response was detected in less than 50% of those infected by vaccine
-no one in the asymptomatic MERS group seroconverted
-among MERS patients with pneumonia, 75% of fatal cases did not seroconvert
-in asymptomatic/mild "SARS-COV-2" group, none had IgM levels and three tested negative for IgG
-a confirmatory Western Blot was not performed in order to understand the INCONSISTENCY of the presence of IgM and IgG
-cross-reaction tests were not performed
-only 58 of 112 "SARS-COV-2" patients had both IgM and IgG antibodies, whereas 7 had neither of them, 1 had IgM but no IgG, and 46 had IgG but no IgM
Taken all together, these studies provide indirect evidence that the unseen hypothetical/theoretical particles known as antibodies can be found in some cases of disease. These studies also provide evidence that these unseen hypothetical/theoretical particles are not found in many cases of disease. Antibodies may be associated with more severe disease but are also not present in cases of severe disease. They may be present in asymptomatic/mild cases of disease but are also not present in many asymptomatic/mild cases of disease. The HAI gold standard of antibody titers > 40 has been correlated with "protection" in a few studies but this level has also been shown to be completely ineffective at providing "protection" in many studies post vaccination.
The problem for Immunology and "antibodies" is that, just as in the case with Virology and "viruses," they rely primarily on correlation equaling causation. However, these correlations are inconsistent at best and many times non-existent and/or contradicted in future studies. Instead of admitting they may be wrong by throwing out the old theories and starting over, they try to cram new, contradictory findings/theories into the existing theory thus creating a nearly incomprehensible and overly confusing mosaic made up of pieces from completely unrelated puzzles.
This is why they can claim antibodies are "protective" even though they are not found in many cases of disease. This is how they can state that antibodies are a sign the immune system is working in regards to vaccinations yet they are also a sign one has a weakened immune system with HIV. This is why the presence of antibodies means one has successfully fought off a disease and will be "protected" from future infections yet in the case of Dengue Fever, antibodies will make a reinfection worse and potentially fatal. This is how we end up with multiple immune systems with factors that can be simultaneously protective and pathogenic.
https://docs.google.com/document/d/e/2PACX-1vThXfZwg1Os5HEfIZE_ThkUohR_I-t4AnhBlCC9Dct6vOzVb8v38IW0KSvQ5tHOwp1lALKwWTLtrrA0/pub
ANTIBODIES ARE NOT REQUIRED FOR IMMUNITY: ?
In 2012, a study came out that completely contradicted the theory that antibodies are required for survival and immunity from "viruses." Knowing what we know about the lack of proof regarding these unseen hypothetical/theoretical particles, it shouldn't come as any surprise that results such as these eventually came about. It is very similar to what Merrill Chase "discovered" in 1942 when his findings broke immunity into the Innate (Cellular) system and the Adaptive (Antibody) system. However, whereas Chase theorized that antibodies still played a role in survival/immunity, newer findings are showing that this is not the case. Here are some excerpts from the ScienceDaily press release on the findings from 2012:
"ANTIBODIES ARE NOT REQUIRED FOR IMMUNITY AGAINST SOME VIRUSES
A NEW STUDY TURNS THE WELL ESTABLISHED THEORY THAT ANTIBODIES ARE REQUIRED FOR ANTIVIRAL IMMUNITY UPSIDE DOWN and reveals that an unexpected partnership between the specific and non-specific divisions of the immune system is critical for fighting some types of viral infections. The research, published online on March 1st in the journal Immunity by Cell Press, may lead to a new understanding of the best way to help protect those exposed to potentially lethal viruses, such as the rabies virus."
"THE RESEARCH TEAM STUDIED VSV INFECTION IN MICE THAT HAD B CELLS BUT DID NOT PRODUCE ANTIBODIES. Unexpectedly, although the B cells themselves were essential, SURVIVAL AFTER VSV EXPOSURE DID NOT REQUIRE ANTIBODIES OR OTHER ASPECTS OF TRADITIONAL ADAPTIVE IMMUNITY. "We determined that the B cells produced a chemical needed to maintain innate immune cells called macrophages. The macrophages produced type I interferons, which were required to prevent fatal VSV invasion," says co-author Dr. Matteo Iannacone.
Taken together, the results show that the essential role of B cells against VSV DOES NOT REQUIRE ADAPTIVE MECHANISMS, but is instead directly linked with the innate immune system. "OUR FINDINGS CONTRADICT THE CURRENT VIEW THAT ANTIBODIES ARE ABSOLUTELY REQUIRED TO SURVIVE INFECTION WITH VIRUSES LIKE VSV, and establish an unexpected function for B cells as custodians of macrophages in antiviral immunity," concludes Dr. von Andrian.
https://www.sciencedaily.com/releases/2012/03/120301143426.htm
Below are highlights from this study:
B CELL MAINTENANCE OF SUBCAPSULAR SINUS MACROPHAGES PROTECTS AGAINST A FATAL VIRAL INFECTION INDEPENDENT OF ADAPTIVE IMMUNITY
ABSTRACT
"NEUTRALIZING ANTIBODIES HAVE BEEN THOUGHT TO BE REQUIRED FOR PROTECTION AGAINST ACUTELY CYTOPATHIC VIRUSES, such as the neurotrophic vesicular stomatitis virus (VSV). UTILIZING MICE THAT POSSESS B CELLS BUT LACK ANTIBODIES, we show here that survival upon subcutaneous (s.c.) VSV challenge was INDEPENDENT OF NEUTRALIZING ANTIBODY PRODUCTION OR CELL-MEDIATED ADAPTIVE IMMUNITY. However, B cells were absolutely required to provide lymphotoxin (LT) α1β2, which maintained a protective subcapsular sinus (SCS) macrophage phenotype within virus draining lymph nodes (LNs). Macrophages within the SCS of B cell-deficient LNs, or of mice that lack LTα1β2 selectively in B cells, displayed an aberrant phenotype, failed to replicate VSV, and therefore did not produce type I interferons, which were required to prevent fatal VSV invasion of intranodal nerves. Thus, although B cells are essential for survival during VSV infection, their contribution involves the provision of innate differentiation and maintenance signals to macrophages, RATHER THAN ADAPTIVE IMMUNE MECHANISMS.
INTRODUCTION
"ADAPTIVE IMMUNITY, ESPECIALLY NEUTRALIZING ANTIBODY PRODUCTION, IS THOUGHT TO PLAY A CRITICAL ROLE IN CONTROLLING CYTOPATHIC VIRAL INFECTIONS IN MAMMALS (Hangartner et al., 2006). However, external barrier breach by rapidly replicating viruses can place a host at risk long before adaptive immune components can be mobilized. Indeed, mice infected with VSV, an acutely cytopathic neurotropic rhabdovirus, CAN SUFFER FATAL NEUROINVASION DESPITE HIGH NEUTRALIZING ANTIBODY TITERS (Iannacone et al., 2010). This observation led us to revisit the contribution of humoral immune responses to survival after VSV infection.
Intravenous (i.v.) infection of mice with VSV elicits neutralizing T cell-independent IgM and T cell-dependent IgG responses that become detectable by days 4 and 7 postinfection, respectively (Bachmann et al 1994, 1996; Charan and Zinkernagel, 1986; Karrer et al., 1997; Thomsen et al., 1997). Because B cell-deficient or CD4+ T cell-deficient mice die after i.v. VSV infection, IT HAD BEEN THOUGHT THAT NEUTRALIZING T CELL-DEPENDENT ANTIBODIES WERE ABSOLUTELY REQUIRED FOR SURVIVAL (Bründler et al., 1996)."
"We have shown recently that the susceptibility to VSV neuro-invasion upon LN macrophage depletion has a fatal outcome in ~60% of infected mice, WITH BOTH DYING AND SURVIVING ANIMALS PRODUCING SIMILAR NEUTRALIZING ANTIBODY TITERS (Iannacone et al., 2010). THUS, HUMORAL IMMUNITY WAS APPARENTLY NOT SUFFICIENT FOR MOST INDIVIDUALS’ SURVIVAL OF s.c. VSV INFECTION, although it remained possible that antibodies afforded viral clearance in the surviving ~40% of mice. To clarify the role of B cells and antibodies and to re-examine the requirements for protection against VSV, we undertook the present study. By utilizing animals that selectively lack antibodies but retain B cells, WE FOUND THAT NEITHER HUMORAL NOR CELL-MEDIATED ADAPTIVE IMMUNITY WERE REQUIRED FOR PROTECTION AGAINST VSV."
"RESULTS
ANTIBODIES, but Not B Cells, ARE DISPENSABLE for Protection against Subcutaneous VSV Infection
Previous studies have shown that B cell-deficient mice are highly susceptible to acutely cytopathic viruses, including VSV (Bachmann et al., 1995; Bründler et al., 1996; Gobet et al., 1988; Hangartner et al., 2006). ALTHOUGH THIS FINDING WAS INTERPRETED AS EVIDENCE THAT ANTIBODIES ARE ABSOLUTELY REQUIRED, it must be considered that B cell-deficient mice NOT ONLY LACK ANTIBODIES but also display abnormal lymphoid architecture (Kitamura et al., 1991). Therefore, WE SOUGHT TO RE-EVALUATE THE RELATIVE CONTRIBUTION OF ANTIBODY-DEPENDENT AND -INDEPENDENT FUNCTIONS OF B CELLS TO PROTECTIVE IMMUNITY AGAINST VSV. We took advantage of a recently generated mouse strain, DHLMP2A, in which the JH segment of the IgH locus was replaced by the Epstein-Barr virus-derived LMP2A protein (Casola et al., 2004). Because LMP2A provides tonic survival signals, B cells develop without a B cell receptor; therefore, DHLMP2A mice retain B cells and normal lymphoid tissue architecture, YET ARE DEVOID OF SURFACE-EXPRESSED AND SECRETED ANTIBODIES.
Consistent with previous studies (Bründler et al., 1996), B cell-deficient (μMT) mice died within 10 days of i.v. infection, whereas WT mice survived the viral challenge (Figure 1A). DHLMP2A mice were also susceptible to death after i.v. VSV infection, with a clinical course and mortality rate that were indistinguishable from those of μMT mice (Figure 1A). However, when mice were challenged s.c. (the natural transmission route for arboviruses, such as VSV [Mead et al., 1999]), ~60% of μMT mice died after developing ascending paralysis. In contrast, DHLMP2A MICE, like WT mice, WERE PROTECTED (Figure 1B), EVEN THOUGH (as expected) THEY WERE INCAPABLE OF MOUNTING A NEUTRALIZING ANTIBODY RESPONSE TO VSV (Figure 1C)."
"Although our results after i.v. viral challenge support an antibody requirement for survival of acutely cytopathic viral infection (Bachmann et al., 1997; Bründler et al., 1996), OUR FINDINGS IN THE s.c. INFECTION MODEL ARE NOT COMPARABLE WITH THIS ANTIBODY-CENTRIC PARADIGM. Rather, our findings in DHLMP2A mice imply that B cells may have an additional innate role in antiviral immunity THAT MUST BE ANTIBODY INDEPENDENT."
"ADAPTIVE IMMUNITY IS DISPENSABLE during Primary SubcutaneousVSV Infection
MOST MACROPHAGE-DEPLETED WT MICE DIED WHEN CHALLENGED s.c. WITH VSV EVEN THOUGH THEY POSSESSED NEUTRALIZING ANTIBODY TITERS THAT WERE MUCH HIGHER THAN IN MACROPHAGE-SUFFICIENT ANIMALS (Iannacone et al., 2010). In fact, ANTIBODY TITERS WERE INDISTINGUISHABLE between macrophage-depleted WT mice that succumbed to VSV infection and those that remained asymptomatic (Figure S4C). Although the mechanism by which CLL-induced macrophage depletion leads to increased antibody titers in this model remains to be determined, these data, together with our findings in DHLMP2A mice, FIRMLY ESTABLISH THAT ANTIBODIES ARE NEITHER REQUIRED NOR SUFFICIENT FOR SURVIVAL OF A PRIMARY s.c. INFECTION WITH VSV.
This observation raised the question whether adaptive immunity mediated by other lymphocytes is required for protection against peripheral VSV infection. Indeed, both T cells (Kündig et al., 1996; Zinkernagel et al., 1978) and a subset of Thy1+ natural killer cells (Paust et al., 2010) can mount virus-specific effector and memory responses against VSV. To address this question, DHLMP2A mice were depleted of these adaptive lymphocytes by administration of Thy1 antibodies, which resulted in greater than 95% loss of circulating T cells (Figures S4D and S4E). REMARKABLY, DESPITE THE COMPLETE LACK OF BOTH HUMORAL AND CELLULAR ADAPTIVE IMMUNITY, ALL anti-Thy1-treated DHLMP2A MICE SURVIVED VSV INFECTION (Figure 7B). This indicates that the innate immune system, particularly the presence of fully differentiated SCS macrophages, provides sufficient protection to clear this acutely cytopathic viral infection WITHOUT THE NEED FOR ADAPTIVE IMMUNITY.
DISCUSSION
THE RESULTS PRESENTED HERE CONTRADICT THE CURRENT VIEW THAT B CELL-DERIVED NEUTRALIZING ANTIBODIES ARE ABSOLUTELY REQUIRED TO SURVIVE A PRIMARY CYTOPATHIC VIRAL INFECTION, such as that caused by VSV. This paradigm arose originally from experiments in B cell-deficient mice (Bachmann et al., 1994, 1997; Bründler et al., 1996; Gobet et al., 1988), which lack antibodies, but also have abnormal lymphoid tissue architecture and altered macrophage phenotype. Our experiments in mice that lack antibodies but possess B cells and normal lymphoid tissues confirm that both B cells and antibodies are critical to survive a systemic infection after i.v. bolus administration of VSV. However, ONLY B CELLS ARE ESSENTIAL WHEN VSV IS ENCOUNTERED VIA THE MORE “NATURAL” s.c. ROUTE, WHEREAS ANTIBODIES ARE NEITHER NEEDED NOR SUFFICIENT FOR PROTECTION."
"Although VSV infections are typically self-limiting in mammals, rabies virus, a close relative, is responsible for >55,000 human deaths every year. NEUTRALIZING ANTIBODIES ARE ALSO BELIEVED TO BE REQUIRED TO SURVIVE RABIES INFECTIONS, as shown by the fact that passive antibody transfer and active vaccination to elicit humoral immunity are standard of care. Although neutralizing antibodies are undoubtedly effective prophylaxis against rhabdoviruses, OUR FINDINGS INDICATE THAT ANTIBODY THERAPY MAY BE INSUFFICIENT TO TREAT EXISTING RHABDOVIRAL INFECTIONS IN NONIMMUNE SUBJECTS, at least in the case of VSV. It is unclear whether this caveat applies also to rabies virus infection, but FAILURES OF BOTH PASSIVE AND ACTIVE VACCINATION AFTER EXPOSURE TO RABIES ARE KNOWN TO OCCUR (Anonymous, 1988). Thus, it will be important to further dissect the role of antibodies and interferon in this disease. In addition, recent years have seen the emergence and/or spread of other arthropod-borne neurotropic viral infections, such as West Nile virus, Japanese encephalitis virus, and Eastern and Western equine encephalitis virus, to name a few (Weaver and Barrett, 2004). It remains to be determined whether the cellular and molecular immunological events that occur upon inoculation of these pathogens in the skin are similar to the ones identified here."
"IN CONTRAST TO THE LIKELY BENEFIT OF ADAPTIVE IMMUNITY DURING REINFECTION, our results demonstrate that during a primary s.c. infection, recognition of viral epitopes by either antibody or TCR is neither necessary nor sufficient to prevent fatal VSV neuroinvasion. THIS OBSERVATION RUNS COUNTER TO THE COMMONLY HELD VIEW THAT DURING VIRAL INFECTIONS, INNATE IMMUNITY MUST ORCHESTRATE THE INDUCTION OF ANTIVIRAL ADAPTIVE RESPONSES TO ACHIEVE STERILIZING IMMUNITY."
"In summary, WE DEMONSTRATE THAT NAIVE MICE CAN SURVIVE a s.c. VSV CHALLENGE WITHOUT REQUIRING ANTIGEN-SPECIFIC ADAPTIVE IMMUNITY. Efficient protection against VSV is provided by SCS macrophages in the draining LNs that rely on contact with follicular B cells expressing LTα1β2 on their surface. The constant exposure to LTα1β2 induces and maintains the protective SCS macrophage phenotype. Consequently, SCS macrophages in B cell-deficient mice or in mice that lack B cell-expressed LTα1β2 display an altered phenotype that resembles that of medullary macrophages, which are not protective in VSV infection. Like medullary macrophages, SCS macrophages that are deprived of LTα1β2 capture lymph-borne VSV but fail to replicate it. Without replication, SCS macrophages do not produce IFN-I that is required to prevent VSV invasion of intranodal nerves. These findings establish a critical innate function for B cells in antiviral immunity. THIS SETTING REQUIRES B CELLS NOT AS A SOURCE OF ANTIBODIES, but as providers of an anatomically restricted maintenance signal and as the day-to-day custodians of macrophage differentiation."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359130/
In Summary:
-neutralizing antibodies were THOUGHT to be needed for protection against cytopathic "viruses"
-the researchers used mice which lacked antibodies and showed survival from "viral" infection was independent of antibodies and the adaptive immune response
-they concluded that B Cells were essential for survival but not antibodies/adaptive immune mechanisms
-they state that adaptive immunity/antibodies are THOUGHT to play a protective role against "viruses"
-however, mice with high antibody titers still succumbed to fatal neuroinvasive outcomes when infected
-they state again that it is THOUGHT that neutralizing antibodies were required for survival
-both dying and surviving animals had similar neutralizing antibody titers thus humoral (antibody) immunity was not essential for survival
-through their experiments they found that NEITHER Humoral nor cell-mediated Adaptive immunity was required for survival
-they state antibodies are dispensable (i.e. able to be replaced or done without)
-mice incapable of producing an antibody response were protected against the "virus"
-their findings were incompatible with the antibody-specific paradigm
-most macrophage-depleted mice died from infection even though they had higher antibody titers than their macrophage-sufficient counterparts
-they state that the data firmly established that antibodies are neither required nor sufficient for survival
-despite the complete lack of BOTH humoral and cellular immunity, all anti-Thy1-treated DHLMP2A mice survived
-the innate system can work without the adaptive/antibody system
-they state that their results contradict the belief that antibodies are required for survival of "viral" infections
-they state that it is BELIEVED that antibodies are required to survive rabies but this is unclear as failures of both passive and active vaccinations after exposure to rabies has occurred
-they claim that their observation runs counter to the commonly held view that during viral infections, innate immunity must orchestrate the induction of antiviral adaptive responses to achieve sterilizing immunity
-they conclude that mice can survive without adaptive (antibody) immunity and that only B cells, not as a source of antibodies, are required for immunity
The 2012 findings that antibodies are not required for immunity were later backed up in a different study from 2016 involving the Dengue "virus." Highlights from this paper below:
ANTIBODIES ARE NOT REQUIRED TO A PROTECTIVE IMMUNE RESPONSE AGAINST DENGUE VIRUS ELICITED IN A MOUSE ENCEPHALITIS MODEL
"GENERATING NEUTRALIZING ANTIBODIES HAVE BEEN CONSIDERED A PREREQUISITE TO CONTROL DENGUE VIRUS (DENV) INFECTION. However, T lymphocytes have also been shown to be important in a protective immune state. In order to investigate the contribution of both humoral and cellular immune responses in DENV immunity, we used an experimental model in which a non-lethal DENV2 strain (ACS46) is used to intracranially prime Balb/C mice which develop protective immunity against a lethal DENV2 strain (JHA1). Primed mice generated envelope-specific antibodies and CD8+ T cell responses targeting mainly non-structural proteins. IMMUNE SERA FROM PROTECTED MICE DID NOT CONFER PASSIVE PROTECTION TO NAÏVE MICE CHALLENGED WITH THE JHA1 STRAIN."
"Severity of symptoms displayed by a DENV infection is highly associated with viremia titers (Horstick et al., 2015, Murgue et al., 2000, Vaughn et al., 2000). Historically, ANTIBODIES CAPABLE OF PREVENTING VIRUS OF INFECTING SUSCEPTIBLE CELLS HAVE BEEN THOUGHT TO REPRESENT THE MAIN AND, PERHAPS, THE SOLE PROTECTION CORRELATE (Guzman and Harris, 2014, Guzman et al., 2010, SABIN, 1952, Whitehead et al., 2007). Such antibodies were extensively demonstrated to be capable of preventing infection of the host cells in vitro (Blaney et al., 2005, Chiang et al., 2012, Guzman et al., 2010, Roehrig et al., 2008, Whitehead et al., 2007, Zhang et al., 2007), either by blocking the binding step of viral particles or by preventing conformational changes in the protein required for membranes fusion in endosome (Teoh et al., 2012), or by inducing a structural disruption of the viral envelope (Cockburn et al., 2012, Lok et al., 2008, Pierson and Kuhn, 2012). This rational was reinforced by reports of in vivo protection mediated by neutralizing antibodies in non-human primate model (Guirakhoo et al., 2004, Guirakhoo et al., 2001, Guirakhoo et al., 2000, Guy et al., 2010), and was adopted in the development of presently tested anti-dengue vaccine formulations which are based on chimeric or live-attenuated viruses which induce neutralizing antibodies to the four serotypes of DENV (Whitehead et al., 2007). In particular, chimeric live attenuated viruses between DENV and yellow fever virus (YFV) were constructed with the aim of inducing high titers of neutralizing antibodies against DENV envelope proteins (Guirakhoo et al., 2001). IN CLINICAL TRIALS CONSIDERABLE TITERS OF NEUTRALIZING ANTIBODIES WERE INDUCED IN VACCINEES VOLUNTEERS (Sabchareon et al., 2012, Villar et al., 2014). UNFORTUNATELY, ESPECIALLY FOR DENV2, THE VACCINE FORMULATION BASED ON THOSE CHIMERIC VIRUSES DID NOT ACHIEVE THE EXPECTED PROTECTIVE EFFICACY IN A PHASE III CLINICAL TRIALS IN DIFFERENT PARTS OF THE WORLD (Sabchareon et al., 2012, Villar et al., 2014)."
"WE FOUND THAT ANTIBODIES GENERATED IN MICE INOCULATED WITH THE ACS46 STRAIN, although capable of neutralizing the virus in vitro, WERE NOT CAPABLE TO CONFER PASSIVE PROTECTION IN THE ENCEPHALITIS MODEL. In contrast, depletion of CD4+ and CD8+ T lymphocytes drastically reduced the protection of ACS46-inoculated mice challenged with the neurovirulent DENV2 strain. Collectively, our results clearly show that cellular immune responses, particularly those targeting non-structural proteins, are specifically involved in the control of DENV infection in the mouse encephalitis model."
"Aiming to access the specific contribution of the humoral immune response to the protection induced by the ACS46 strain, we carried out in vivo serum transfer experiments. First, envelope-specific IgG titers were determined by ELISA in both serum and brain macerate from mice which were protected from the lethal challenge with the JHA1 strain. We found that envelope-specific antibodies were not present in brain macerate but only in sera (Fig. 4A). Thus, sera from protected mice were administered to naive mice in one, two or three doses. The transfer regimen with three doses resulted in in vivo envelope-specific IgG titers statistically indistinguishable from those found in donor animals (Fig. 4B). ALTHOUGH SERA FROM PROTECTED MICE SHOWED A MINIMUM PRNT50 TITER OF 1:40, WE OBSERVED THAT ITS TRANSFER IN ONE, TWO OR THREE DOSES DID NOT CONFER NEITHER PROTECTION FROM NOR EXACERBATION OF INFECTION UNDER A LETHAL CHALLENGE WITH 100 PFU of the JHA1 strain (Fig. 4C). The lethality curves of animals treated with antibodies from mock or ACS46-primed mice were indistinguishable.
On the other hand, IFN-γ-secreting CD8+ T lymphocytes specific to NS1, NS3H and NS5 DENV2 proteins were significantly increased in ACS46-primed mice (Fig. 5A and 😎. Moreover, when CD4+, CD8+ or both populations of T lymphocytes were depleted from ACS46-primed mice the protective immunity was significantly reduced or completely abrogated (Figs. 5C and 6). THESE RESULTS INDICATE THAT ANTI-ENVELOPE ANTIBODIES INDUCED IN THE MOUSE ENCEPHALITIS MODEL DO NOT CONTRIBUTE TO PROTECTION, but T lymphocytes specific responses, particularly those for non-structural proteins, play major roles in controlling virus replication and prevention of encephalitis."
"Discussion
A very large number of people are infected by any of the DENV serotypes per year and a significant portion of them develop severe forms of dengue. Despite the significant epidemiological effect of this disease, there is not an effective anti-DENV vaccine formulation approved for use in humans. Relevantly, AN IMPORTANT VACCINE FORMULATION DESIGNED TO INDUCE GENERATION OF NEUTRALIZING ANTIBODIES DID NOT ACHIEVE THE EXPECTED PROTECTIVE EFFICACY IN A PHASE III CLINICAL TRIAL, especially against serotype 2 (Sabchareon et al., 2012, Villar et al., 2014). In other words, THE CORRELATE OF PROTECTION PROPOSED SEVEN DECADES AGO FOR DENV INFECTION SEEMS TO BE INCOMPLETE, AND THE NEED TO REFORMULATE IT IS CLEAR. In this study we found ANTIBODIES GENERATED IN A PROTECTIVE IMMUNITY INDUCED IN A Balb/C ENCEPHALITIS MODEL ARE NOT CAPABLE TO CONTROL IN VIVO ENCEPHALITIS CAUSED BY DENV2. However, CD4+ and CD8+ T lymphocytes are crucial in our experimental model. In addition, CD8+/IFN+ T lymphocytes targeting non-structural proteins are present in significantly increased levels in animals capable of controlling infection and play major roles in controlling encephalitis. Together, RESULTS PRESENTED IN THIS STUDY SHOWED THAT ANTIBODIES ARE NOT CAPABLE ALONE TO ESTABLISH PROTECTIVE IMMUNITY TO DENV2 in the Balb/C mouse encephalitis model."
"Another study has investigated the role of humoral versus cellular responses induced by a protective anti-DENV vaccine (Zellweger et al., 2013). IN THIS STUDY THE HUMORAL COMPONENT BY ITSELF WAS SHOWN TO BE UNABLE TO CONTROL THE INFECTION OF IMMUNE DEFICIENT MICE (AG129) with a DENV2 strain after intravenous administration."
"Even though this experimental infection model does not resemble the context of the infection seen in humans, it represents another clear evidence that the control of DENV infection requires the involvement of T cell responses, particularly to non-structural proteins. RESULTS PRESENTED IN THIS STUDY FURTHER REINFORCE THE NEED TO REEVALUATE THE ROLE OF ANTIBODIES AS THE UNIQUE PARAMETER INVOLVED IN DENV INFECTION."
"Notably, these two subsets of T lymphocytes were shown to control infection WITHOUT REQUIREMENT OF ANTIBODIES, which again recall data generated with i.m. immunization, in which ENVELOPE-SPECIFIC ANTIBODIES ARE NOT CAPABLE TO CONTROL ENCEPHALITIS. Thus, THE PROTECTIVE IMMUNE RESPONSE OBSERVED IN OUR MODEL AND HEADED BY T LYMPHOCYTES DOES NOT SEEM TO REQUIRE THE TRIGGERING OF VIRAL ENVELOPE ANTIGENS, AT LEAST WITH REGARD TO INDUCTION OF ANTIBODY RESPONSES."
https://www.sciencedirect.com/.../pii/S004268221500433X
In Summary:
-the generation of antibodies was CONSIDERED to be a prerequisite to control Dengue fever
-the immune sera from protected mice did not transfer passive (antibody) immunity to naive mice
-antibodies were THOUGHT to be the main, and sole, protective correlate
-in clinical trials, neutralizing antibodies were generated in vaccinated volunteers but this had no protective effect
-antibodies generated in mice were incapable of providing a protective effect
-even though antibodies were generated, its transfer in 1, 2, and 3 doses did not pass on protective effects nor exacerbation of infection under lethal challenge trials
-they state that their results show that antibodies did not contribute to protection
-a vaccine formulated to induce generation of neutralizing antibodies did not achieve protective efficacy
-they state that the correlate of protection proposed seven decades ago was incomplete and needed to be reformulated
-the antibodies generated in their study were unable to control encephalitis caused by DENV2
-a separate study also showed that humoral immunity alone was incapable of protecting immune-deficient mice
-they state that their results show that the role of antibodies needed to be reevaluated
-their results show that T lymphocytes can control infection without antibodies, which were not capable of controlling encephalitis
-they conclude that the protective immune response observed does not seem to require the triggering of viral envelope antigens, at least with regard to induction of antibody responses
These two studies show that the theoretical particles claimed to be antibodies are not a requirement for immunity nor protection. The results completely contradict the main theories regarding the function and role of antibodies in supposed immunity. Maybe the fact that these studies were unable to find a protective effect from antibodies goes a ways towards explaining how one can be considered HIV positive if antibodies are detected. Maybe it explains how having too many antibodies can be associated with an overactive immune system while too few antibodies is associated with a weakened immune system. Maybe it helps to explain why a second infection with Dengue fever is worse than the first and that the resulting antibodies are blamed for triggering life-threatening infections. Maybe it just goes to show that they truly have no idea what these unseen hypothetical/theoretical particles are, how they function, or if they even exist to begin with. One thing that is certain is that, when it comes to the theories about antibodies, they are not certain about anything at all. When nothing is for certain, any contradicting hypothesis or theory will seem possible.
https://docs.google.com/document/d/e/2PACX-1vQ2ipqUmdXnH_5gRwwPuUSxxzHx8MJrvvMyWx-AUpOg5acEx3rDlt9QNJUI5DmKA6biMCa8ciuHpnu-/pub
It's not looking too good for the claim of antibody SPECIFICITY…
HEADLINE: More evidence suggests COVID-19 was in US by Christmas 2019
HIGHLIGHTS:
"Like the CDC study, THESE RESEARCHERS LOOKED FOR ANTIBODIES IN THE BLOOD that are taken as evidence of coronavirus infection, and can be detected as early as two weeks after a person is first infected.
The researchers say seven study participants — three from Illinois, and one each from Massachusetts, Mississippi, Pennsylvania, and Wisconsin — were infected earlier than any COVID-19 case was originally reported in those states.
One of the Illinois cases was infected as early as Christmas Eve, said Keri Althoff, an associate professor at the Johns Hopkins Bloomberg School of Public Health and the study's lead author.
IT CAN BE DIFFICULT TO DISTINGUISH ANTIBODIES THAT NEUTRALIZE SARS-CoV-2, THE VIRUS THAT CAUSES COVID-19, FROM ANTIBODIES THAT FIGHT OTHER CORONAVIRUSES, INCLUDING SOME THAT CAUSE THE COMMON COLD. Researchers in both the NIH and CDC studies used multiple types of tests to minimize false positive results, BUT SOME EXPERTS SAY IT STILL IS POSSIBLE THEIR 2019 POSITIVES WERE INFECTIONS BY OTHER CORONAVIRUSES AND NOT THE PANDEMIC STRAIN."
https://www.yahoo.com/news/more-evidence-suggests-covid-19-133445284.html
So antibodies are "specific"...except they are not. If they can't tell one "coronavirus" from another one, how are these tests being used today to claim one either had the "virus" or that the vaccines are inducing the right antibodies for the right "virus?"
When you realize both "viruses" and "antibodies" have never been properly purified/isolated nor proven to exist, you realize the results of these tests and the data coming from them are absolutely MEANINGLESS.
https://docs.google.com/document/d/e/2PACX-1vTWyCcuRdv-WP7g4c31FUaCN8EavnKqnezaymD9Mcfn-_CmXrJlJygDfsipRFwh1pcblvb_iKe-YeF5/pub
ANTIBODY SPECIFICITY?:
"NO, THERE IS NO SUCH THING AS A MONOCLONAL ANTIBODY THAT, because it is monoclonal, RECOGNIZES ONLY ONE PROTEIN OR ONLY ONE VIRUS. It will bind to ANY PROTEIN having the same (or a very similar) sequence."
- Clifford Saper, one of the world’s leading authorities on monoclonal antibodies, Harvard Medical School professor
https://off-guardian.org/2021/03/06/the-antibody-deception/
In 2005, Clifford Saper wrote an open letter to the readers of the Journal of Comparative Neurology. In it, he described the problems facing antibody research: mainly the lack of specificity and the inability to reproduce results. He laid forth some criteria that needed to be met in his letter as well as in future papers he published. A few highlights from the letter:
"The Journal has repeatedly, over the last few years, RECEIVED DISTRESSED COMMUNICATIONS FROM AUTHORS, WHO HAVE HAD TO WITHDRAW PAPERS BECAUSE AN ANTIBODY AGAINST A NOVEL MARKER WAS FOUND TO STAIN TISSUE IN KNOCKOUT ANIMALS, WHO LACK THAT TARGET PROTEIN. In many cases these papers contained careful characterization of the antibodies and immunocytochemical controls. THIS ISSUE HAS SENSITIZED THE EDITORS TO THE PROBLEM OF ANTIBODY SPECIFICITY, and we soon realized that many of the papers we were publishing had VERY LIMITED CHARACTERIZATION OR CONTROLS FOR ANTIBODIES THAT WERE USED."
"It is important to recognize that ANTIBODIES ARE NOT SIMPLE REAGENTS THAT ALWAYS IDENTIFY THE SAME THING."
doi: 10.1002/cne.20839.
A little more background info on Saper's findings from the Nature article ANTIBODY ANARCHY: A CALL TO ORDER:
"A MOUSE FIRST ALERTED CLIFFORD SAPER TO THE FACT THAT ANTIBODIES WERE MISLEADING THE SCIENTIFIC COMMUNITY. As editor-in-chief of the Journal of Comparative Neurology between 1994 and 2011, he handled scores of papers in which scientists relied on antibodies to flag the locations of neurotransmitters and their receptors. Around the turn of the century, related investigations began to roll in from researchers using knockout mice, animals genetically engineered to not express a target gene. THE RESULTS WERE UNSETTLING. Antibody staining in knockout animals SHOULD HAVE SHOWN RADICALLY DIFFERENT PATTERNS from those in unmodified animals. BUT ALL TOO OFTEN THE IMAGES WERE IDENTICAL. “As we saw MORE AND MORE RETRACTIONS DUE TO THIS, I began to realize that we had NO SYSTEMATIC WAY TO EVALUATE PAPERS THAT USED ANTIBODIES,” recalls Saper, now chair of neurology at Beth Israel Deaconess Medical Center in Boston, Massachusetts."
"Today, biomedical researchers still collect tales of antibody woe faster than country-music labels spin out sad songs. The most common grumble is the cheating reagent: THE ANTIBODY PURCHASED TO DETECT PROTEIN X SURREPTITIOUSLY BINDS PROTEIN Y (AND PERHAPS IGNORES X ALTOGETHER). Another complaint is 'lost treasure': a run of promising experiments that stalls when a new batch of antibodies FAILS TO REPRODUCE PREVIOUS FINDINGS (see 'A market in a bind')."
"It is alarming, then, to discover that ANTIBODIES CAN BE UNRELIABLE REAGENTS. INSUFFICIENT SPECIFICITY, SENSITIVITY AND LOT-TO-LOT CONSISTENCY have resulted in false findings and wasted efforts."
https://www.nature.com/articles/527545a?proof=t
Below are highlights from two separate reviews Saper published regarding the antibody specificity and reproducibility problems:
A GUIDE TO THE PERPLEXED ON THE SPECIFICITY OF ANTIBODIES
"MANY INVESTIGATORS ARE UNAWARE OF THE POTENTIAL PROBLEMS WITH SPECIFICITY OF ANTIBODIES and the need to document antibody characterization meticulously for each antibody that is used."
"Since the description of indirect immunohistochemical (IHC) staining by Coons (1958), IHC staining has become a standard method used in most laboratories doing cellular or systems level localization of proteins and other cellular constituents. In fact, the methods have become so mundane that many current practitioners take for granted that an antibody that is sold to localize a particular molecular target will be both sensitive and specific. In the current era of very accurate DNA analyses by in situ hybridization, DNA chip analyses, and deep sequencing, IT IS OFTEN ASSUMED THAT IHC HAS AN ANALOGOUS ABILITY TO IDENTIFY MOLECULAR TARGETS ACCURATELY.
NOTHING COULD BE FURTHER FROM THE TRUTH.
In fact, IHC METHODS REMAIN AS PRIMITIVE, IN TERMS OF BOTH SENSITIVITY AND SPECIFICITY, as they were in the days when DNA sequencing was done by hand using sequencing gels. THE FUNDAMENTAL PRINCIPLES on which antibody localization is based HAVE NOT IMPROVED AT ALL IN THE LAST TWO DECADES, and if anything, THE SLOPE OCCUPIED BY IHC HAS BECOME MORE SLIPPERY THAN EVER."
"By fusing individual antibody-producing cells with antibody-producing myeloma cells, individual cells can be immortalized, so that they divide into colonies of “hybridoma” cells, all of which produce the same, identical immune globulin, with the same variable region. These monoclonal antibodies have the property that they will only bind to molecules that bind that single variable site. Although this relationship imparts specificity to the interaction, IT IS POSSIBLE THAT THE VARIABLE SITE MAY BIND TO A VARIETY OF DIFFERENT TARGETS, particularly when tested in different tissues, and that THESE MAY BE QUITE DIFFERENT FROM THE MOLECULE AGAINST WHICH THE ANTIBODY WAS RAISED."
"Monoclonal Antibodies vs Polyclonal Antisera
As indicated above, access to monoclonal antibodies has provided us with antibodies that are pure reagents. The monoclonal antibodies are derived from hybridoma cells, WHICH ARE GROWN EITHER IN CULTURE OR BY INJECTING THEM INTRAPERITONEALLY IN A HOST ANIMAL. When the hybridoma cells are grown intraperitoneally, the host animals build up fluid, which is called ascites and which can be drawn off from the abdomen and contains high concentrations of the monoclonal antibodies. Either the culture fluid or ascites fluid containing the antibodies can be subjected to purification by precipitating the antibodies with protein A. The resulting RELATIVELY PURE antibody preparations are quantified based on the micrograms of protein.
Polyclonal antisera, in contrast, are derived by bleeding animals a few weeks after they have been immunized. Usually several “booster immunizations” are given, and several bleeds are taken. Blood volume in a mammal is usually ∼7% of body weight, and typically ∼10–15% of total blood volume may be exsanguinated at any one time without injury to the animal. Hence, a single bleed from a 3-kg rabbit may be 25 ml, whereas a bleed from a 30-kg goat can be 250 ml. When the red blood cells are spun down from the clotted blood, the remaining serum is usually about one half this volume. As a result, a single bleed from a larger animal can be used for a much larger number of IHC reactions than a bleed from a smaller animal. The advantage of having the larger amount of serum per bleed is that each bleed is essentially a unique combination of antibody clones. EVEN WHEN BOOSTING THE SAME ANIMAL WITH REPEATED IMMUNIZATIONS WITH THE SAME ANTIGEN, THE ANTIBODY CONTENT IN SEQUENTIAL BLEEDS MAY DIFFER MARKEDLY. Hence, the lot for a polyclonal antiserum is critical, AND EVEN ANOTHER BATCH FROM THE SAME ANIMAL MAY HAVE ENTIRELY DIFFERENT STAINING PROPERTIES. For this reason, experienced immunohistochemistry write down the lot numbers for each vial of antiserum and, when they have a good lot, buy up as much of that lot as they are likely to need in the foreseeable future to avoid inability to finish a project.``
"Synthetic Peptide Antigens and Antigen Mapping
THE ABILITY TO CREATE SYNTHETIC PROTEINS AND PEPTIDES HAS REVOLUTIONIZED THE WAY IN WHICH ANTIBODIES MAY BE MADE and how they can be characterized. Synthetic peptides are usually from a few amino acids up to ∼25 or 30 in length. The current peptide synthesis technology results in decreasing yields as the peptide lengthens, so that synthetic peptides much longer than this, while possible, are not practical. On the other hand, much longer amino acid sequences can be prepared by recombinant technology, in which a corresponding nucleic acid sequence is expressed either in a cellular or cell-free protein expression system. It seems obvious that the exact sequence used to create the antibody is critical to its properties, and hence, we will return to this issue in the criteria for antibody suitability.
At the same time, the availability of amino acid sequences from different parts of the parent target molecule has allowed us to identify the target sites in the native molecule to which the antibody binds. When the antibody binds to a partial sequence or a partial sequence competes against binding to the native molecule, THE EPITOPE, or structural features that the antibody recognizes, IS PRESUMED TO BE LOCATED IN THAT SEQUENCE. This method is used to map the epitope that the antibody binds. HOWEVER, THIS DOES NOT INDICATE WHAT THE SEQUENCE WAS OF THE ORIGINAL IMMUNOGEN, BECAUSE THE ANTIBODY MAY HAVE BEEN MADE AGAINST AN OVERLAPPING SEQUENCE."
"Antibodies Against Different Portions of the Same Molecule
A related topic is the ability to generate antibodies against synthetic peptides that are derived from different components of the same molecule. Thus, it is possible, for example, to have antibodies against a large protein target that specifically bind to the N- or the C-terminal portions of the protein. This possibility gives us a powerful potential tool to use in determining antibody specificity. When the two different antibodies stain exactly the same pattern, IT IS HIGHLY LIKELY THAT THEY ARE STAINING THE CORRECT TARGET.
Antibodies Against Phosphorylated or Glycosylated Epitopes
Another possibility provided by the use of synthetic antigens is to prepare immunogens that are specifically altered, for example, with phosphorylation, glycosylation, or some other post-translational modification. Antibodies prepared in this way MAY BE ABLE to distinguish between different modified forms of the same molecule with great accuracy. However, SHOWING THIS SPECIFICITY REQUIRES APPROPRIATE CONTROLS (such as staining after dephosphorylation)."
"Rules for Judging Whether an Antibody Is Showing What Is Expected in Tissue
MOST INVESTIGATORS WANT TO USE ANTIBODIES TO LOCALIZE CELLULAR COMPONENTS AND DO NOT WANT TO HAVE TO BECOME EXPERTS IN IMMUNOLOGY OR IHC to do so. Hence, it is useful to have a set of criteria for what constitutes A REASONABLE DEGREE OF ASSURANCE THAT THE ANTIBODY BEING USED IS ACTUALLY TARGETING ITS CORRECT ANTIGEN. The answers to the questions that follow are ones that investigators should ask for each antibody they are acquiring, before they ever use it in an experiment (why waste time on an invalid antibody?). IF ALL INVESTIGATORS FOLLOWED THESE RULES, THE LITERATURE WOULD BE MUCH MORE ACCURATE, AND INVESTIGATORS WOULD AVOID WASTING A LOT OF TIME ON INVALID ANTIBODIES.
What Immunogen Is Used to Raise the Antibody?
The first critical criterion in locating a valid antibody is that the immunogen against which the antibody was raised must be known. A KEY PRINCIPLE OF SCIENCE IS THAT THE WORK MUST BE REPEATABLE. Hence, IF THE ANTIBODY IS RAISED AGAINST A “PROPRIETARY” ANTIGEN (USUALLY A SECRET AMINO ACID SEQUENCE, to avoid competitors from copying the product), IT SIMPLY IS NOT VALID FOR SERIOUS SCIENTIFIC WORK. Some manufacturers have claimed that their “intellectual property” must be protected if they are to provide antibodies in the future, but in fact, this has become a routine process, and for most antibodies there are multiple manufacturers who do provide the sequence for their antigens. More importantly, if protecting their profits interferes with science, it is the use of their product that must be eliminated. Other manufacturers have claimed that they will provide their proprietary product to other laboratories in the future, so that the result of the experiment is repeatable. However, there is tremendous turnover in this field, and COMPANIES FRANKLY ARE IN BUSINESS TO MAKE PROFITS AND NOT TO PROTECT SCIENTIFIC INTEGRITY. If they find tomorrow morning that they can make more profit selling shoes than antibodies, that is exactly what they will do, AND NO ONE WILL BE ABLE TO REPEAT THE WORK. Hence, a key issue in buying any new antibody is to avoid products for which the identity of the immunogen is not provided at the time it is purchased.
What is the Evidence That the Antibody Binds Specifically to the Expected Target Molecule in the Tissue of Interest?
The second key criterion for using an antibody in a scientific project should be TO OBTAIN AT LEAST REASONABLE EVIDENCE THAT THE ANTIBODY DOES BIND TO ITS EXPECTED TARGET IN THE TISSUE IN WHICH IT WILL BE STUDIED AND NOT TO SOMETHING ELSE. This is often provided by a Western blot, which should show that the antibody stains a single band (or a set of bands) of appropriate molecular mass for that target. Note that IF EXTRANEOUS BANDS ARE STAINED, THIS INDICATES THAT THE ANTIBODY HAS OTHER ADDITIONAL TARGETS in the tissue and should raise red flags against using that antibody for IHC, unless you have taken additional precautions."
"Note the importance of doing the Western blot in the same tissue and species as the antibody will be applied for IHC. IT IS QUITE POSSIBLE FOR THE ANTIBODY TO SEE ONLY ONE BAND IN SOME TISSUES BUT TO SEE MULTIPLE EXTRANEOUS BANDS IN OTHER TISSUES FROM THE SAME ANIMAL. Similarly, manufacturers often try to “PROVE” specificity by running the antibody against a gel preparation of purified or recombinant protein. This may show that the antibody can bind to its target BUT DOES NOT TELL ANYTHING ABOUT WHAT ELSE IT MAY BIND TO IN TISSUE."
"What Controls Can Be Done to Insure That the Antibody Binds in Fixed Tissue Only to Its Target Molecule?
Despite our best attempts to insure specificity of the antibody against native proteins in the aqueous phase, ultimately we have to apply it to fixed tissue. IN THE FIXED STATE, IT IS POSSIBLE THAT THE ANTIBODY THAT WORKS WELL IN A WESTERN BLOT WILL FIND THAT ITS TARGET ANTIGEN IS DISTORTED BY THE FIXATION PROCESS AND NO LONGER RECOGNIZABLE. In fact, THIS OCCURS SO OFTEN THAT MOST MANUFACTURERS MARK ANTISERA AS USABLE for Western blotting or IHC, AND THE LATTER ARE BY FAR THE RARER.
When polyclonal antisera are raised against a peptide antigen, it is common that most of the antisera that are produced will stain fixed tissue poorly or not at all. In one case in which the author screened antisera, WE FOUND ONLY 2 OF 31 AGAINST A COMMON PEPTIDE HORMONE THAT COULD BE USED TO STAIN BRAIN TISSUE. If one applies the mathematics of a Poisson distribution to this problem (i.e., ASSUME THAT THE PROBABILITY OF STIMULATING A SINGLE ANTIBODY CLONE THAT RECOGNIZES THE FIXED MOLECULE IS AN INDEPENDENT EVENT), it is likely that, in most polyclonal sera, the antiserum is staining the tissue with only one or at most a small number of antibody clones (i.e., that the polyclonal, WHICH MAY CONTAIN THOUSANDS OF CLONES AGAINST OTHER ANTIGENS the host animal encountered in its lifetime, is functionally a monoclonal or oligoclonal for this purpose)."
"One of the best tests to show that the antibody can identify its target in fixed tissue is to transfect the DNA for the target protein into cells that normally do not make it in tissue culture. The transfected and untransfected controls can then both be fixed and stained, and the presence of staining in the transfected cells shows that the antibody really does stain its target. However, THIS CONTROL DOES NOT PROVE THAT THE ANTIBODY WILL ONLY STAIN ITS TARGET IN THE TISSUE OF INTEREST.
Another control for specific staining in tissue is the preadsorption test. Mixing the diluted antibody with an excess of the immunogen should completely block staining. This shows that the staining in the tissue is against something that is at least cross-reactive with the original protein (ALTHOUGH IT DOES NOT PROVE THAT THIS IS WHAT THE TARGET IN THE TISSUE ACTUALLY IS). In general, when the original immunogen is readily available, such as for a synthetic peptide, the preadsorption test should be run as a matter of course. This is less practical for large protein molecules and antibodies against partially purified tissue components. NOTE THAT THE PREADSORPTION CONTROL IS MEANINGLESS FOR A MONOCLONAL ANTIBODY (which is produced by screening for its binding to the target, and therefore will always bind it and always pass a pre adsorption test, by definition) and for antibodies that have already been affinity purified (for the same reason).
As a practical matter, the best controls for assuring that the staining in the tissue is the target molecule involve one of two approaches (Lorincz and Nusser 2008). First, if the staining is being evaluated in mice or a closely related rodent species, and there is a strain in which the target molecule is deleted, the absence of staining is a strong confirmation of specificity. UNFORTUNATELY, THIS IS NOT A PERFECT TEST, BECAUSE THE TARGET THAT IS STAINED IN THE TISSUE MAY BE A RELATED MOLECULE THAT IS DOWNREGULATED IN THE KNOCKOUT ANIMAL. In addition, this approach only applies to situations where there is a knockout strategy available, WHICH LIMITS IT TO A FEW MODELS SPECIES. Finally, in many so-called knockout mice, the original protein is not entirely eliminated. If only a portion of that protein is still expressed, IT MAY HAVE NO FUNCTIONAL PRESENCE BUT STILL STAIN WITH YOUR ANTIBODY. Hence, it is critical in a knockout control to make sure what the actual gene construct is and what is actually expressed.
The second molecular approach to confirming identity of the staining was alluded to above in the section on making antibodies against different components of the same target molecule. When the two antibodies are made in the same species, SHOWING THAT THE STAINING PATTERNS ARE VERY SIMILAR is a strong control. When the two antibodies are made in different species, simultaneous staining and showing colocalization is an even more satisfying and persuasive control."
"At the same time, we are always uncovering new ways that nature can fool us. Thus, NO ANTIBODY LOCALIZATION IS REALLY PERFECT, although following the practical guide provided here should help investigators, especially those who are new to the mysteries of IHC, to insure the scientific integrity of their work."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605712/
In Summary (Part 1):
-many investigators are unaware of the problems regarding antibody specificity
-it is ASSUMED that immunohistochemical (IHC) staining can identify molecular targets accurately yet he states nothing could be further from the truth
-IHC remains primitive in regards to both sensitivity and specificity
-IHC has not improved in the last two decades
-with monoclonal antibodies, it is possible that the variable site may bind to a variety of different targets
-these may be quite different from the molecule against which the antibody was raised.
-monoclonal antibodies are either grown in culture or grown in animals injected intraperitoneally
-with polyclonal antibodies, even when boosting the same animal with repeated immunizations with the same antigen, the antibody content in sequential bleeds may differ markedly
-batches from the same animal may have entirely different staining patterns
-SYNTHETIC peptides and proteins have "revolutionized" the way antibodies are MADE
-the epitope, or structural features that the antibody recognizes, is PRESUMED to be located in the sequence
-this method does not indicate what sequence was of the original immunogen, because the antibody may have been made against an overlapping sequence
-most investigators want to use antibodies to localize cellular components and do not want to have to become experts in Immunology or IHC
-it is useful to have a set of criteria for what constitutes a reasonable degree of assurance that the ANTIBODY BEING USED IS ACTUALLY TARGETING ITS CORRECT ANTIGEN
-if investigators followed the rules, the literature would be much more accurate and time would not be wasted on INVALID antibodies
-a key principle in science is REPRODUCIBILITY of the work
-if the antibody is raised against a secretive "proprietary" antigen (to avoid competitors from copying the product), it is not valid for serious scientific work
-most companies only care for profits rather than scientific integrity
-keeping these "proprietary" products secretive means no one can reproduce the work
-a second criterion is to obtain AT LEAST REASONABLE EVIDENCE that the antibody does bind to its expected target in the tissue in which it will be studied AND NOT TO SOMETHING ELSE
-if extraneous bands are stained, this indicates that the antibody HAS OTHER ADDITIONAL TARGETS
-it is possible for the antibody to see only one band in a tissue yet see multiple extraneous bands in other tissues from the same animal
-manufacturers try to "prove" specificity by testing against gel or recombinant proteins but this will not tell what other bands an antibody might bind to
-in a fixed state, the antibody may find the antigen is distorted by the fixation process and becomes unrecognizable
-when polyclonal antisera are raised against a peptide antigen, it is common that most of the antisera that are produced will stain fixed tissue POORLY OR NOT AT ALL
-only 2 of 31 polyclonal antisera used against a common peptide could stain brain tissue
-polyclonal antibodies may contain thousands of clones against other antigens
-transfected and untransfected controls do not prove that the antibody will only stain its target in the tissue of interest
-the preadsorption control test does not prove that this is what the target in the tissue actually is
-the preadsorption control is MEANINGLESS for a monoclonal antibody
-the best control is the absence of staining yet this is not a perfect test because the target that is stained in the tissue may be a related molecule that is downregulated in the knockout animal
-he concludes that no antibody localization is perfect
ANTIBODY VALIDATION FOR PROTEIN EXPRESSION ON TISSUE SLIDES: A PROTOCOL FOR IMMUNOHISTOCHEMISTRY
"Antibodies play a crucial role in basic research and clinical decision-making. However, THERE ARE NO STANDARDIZED ALGORITHMS OR GUIDELINES TO ENSURE THEIR ACCURACY AND VALIDITY. There have been efforts to generate consensus, but, with the exception of clinical labs, ANTIBODY VALIDATION REMAINS VARIABLE IN THE LITERATURE AND SOMETIMES IN CLINICAL PRACTICE."
"Data from the Human Protein Atlas indicate that AT LEAST 50% OF OVER 2500 COMMERCIALLY AVAILABLE ANTIBODIES DID NOT PERFORM AS EXPECTED IN THEIR INTENDED ASSAY [2]. Improperly validated antibodies, such as several which target estrogen receptor β, have led to non rigorous research in promising fields [3]."
"The FDA defines validation as ‘the collection and evaluation of data, from the process design stage through commercial production, which establishes scientific evidence that a process is capable of consistently delivering quality product’. In 2014, Fitzgibbons et al. developed laboratory practice guidelines for analytical validation and revalidation of IHC assays used in anatomic pathology clinical services [6]. Still, IT IS ESTIMATED THAT ONLY 52% OF LABORATORIES HAVE ADOPTED SOME OR ALL OF THE RECOMMENDATIONS [7]. Sfanos et al. explained that much of the ‘REPRODUCIBILITY CRISIS’ INVOLVED WITH ANTIBODY USE in IHC stems from END USERS BEING UNAWARE OF THE NEED TO PROPERLY VALIDATE AN ANTIBODY."
"The best antibodies have a very high affinity and very low cross-reactivity. It is also beneficial for them to have a fast on-rate and slow off-rate. However, EVEN WITH RECOMBINANT METHODS, IT IS HARD AND EXPENSIVE TO MAKE A PERFECT ANTIBODY, especially for use in IHC; these assays in particular involve unique conditions for antigens, as tissue fixation can hide epitopes exposed in native or denatured forms and expose epitopes that are not exposed when the protein is in its native form in vivo [10,11]."
"For long-term use in a diagnostic test, and even for reproducible scientific studies, monoclonal antibodies are the best choice. POLYCLONAL ANTIBODIES are produced by several B-cell clones and essentially REPRESENT A POOL OF DIFFERENT ANTIBODY CLONES, each binding to a distinct epitope on the target antigen. While they may be good for rapid proof-of-concept studies, THEY REPRESENT A BATCH-SPECIFIC MIX THAT WILL ULTIMATELY BE EXHAUSTED AND IS THEN IMPOSSIBLE TO REPRODUCE EXACTLY."
"As has been shown, however, MONOCLONAL ANTIBODIES DIRECTED AT A TARGET ARE NOT ALL DEVOID OF THEIR OWN SPECIFICITY AND REPRODUCIBILITY ISSUES, and care must be taken in selecting the best monoclonal antibody, which should always be validated before use [12,13]."
"The first step toward antibody validation consists of demonstrating the expected localization of signal (Figure 2A). While this step was not included in Uhlen et al., we have found it is a critical first step in the IHC validation process. Based on current literature, WE FORM A HYPOTHESIS FOR THE EXPECTED LOCALIZATION OF EXPRESSION OF THE TARGET OF INTEREST. This hypothesis describes the anticipated tissue type (e.g., non-small-cell lung cancer vs breast cancer), histologic subtype (e.g., squamous cell carcinoma vs adenocarcinoma), and cellular (tumor vs stroma) and subcellular (cytoplasmic, membranous or nuclear) localizations of the signal. These hypotheses are based on published literature related to the marker, or data on mRNA from the Cancer Genome Atlas or similar online resources [16]. Generally, more than one source is helpful because RNA does not always correspond to protein. For example, if we were interested in EGFR antibodies, we would typically expect the candidate molecules to show a membranous staining pattern of tumor cells or cell lines known to overexpress EGFR based on mRNA data [17,18]. Because the candidate antibody has not yet been titrated, we often just select the vendor's recommended concentration for a first screen. Investigators should be extra cautious at this step, as APPLICATION OF THE CANDIDATE ANTIBODY IN SUBSTANTIALLY INCREASED CONCENTRATION MAY RESULT IN NONSPECIFIC STAINING PATTERNS (see Step 2)."
"ANTIBODY REPRODUCIBILITY IS A CRITICAL STEP FOR VALIDATION of any antibody to standardize an IHC assay, but was not mentioned as a pillar by Uhlen et al."
"ANTIBODY REPRODUCIBILITY CAN SOMETIMES BE CHALLENGING TO PROVE if the target is heterogeneously expressed in the target tissue."
"While reporting sequences seems like a good idea from a scientific perspective, MANY COMMERCIAL VENDORS POINT OUT THAT THE EPITOPE IS THE ‘SECRET SAUCE’ THAT MAKES THEIR ANTIBODY BETTER THAN OTHER COMPETITORS. Rather than try to patent each epitope (which is not economically feasible), they maintain confidentiality about their epitope and its sequence [44]."
"Because RESEARCH LABS in the academic sector ARE NOT SUBJECT TO ANY CERTIFICATION AND PEER REVIEW IS THE ONLY ‘REGULATORY BODY’ in that sphere, it is perhaps unrealistic to expect strict adherence to any standardization requirements."
"Another key concept likely to be important in IHC in the future is antibody biochemistry. In general, THE AFFINITY AND DISSOCIATION CONSTANTS FOR MOST MONOCLONAL ANTIBODIES ARE NOT KNOWN OR NOT EASILY AVAILABLE. Optimal antibodies for IHC have a fast on-rate and slow off-rate, but the kinetics of antibody binding for IHC are essentially NEVER PUBLISHED."
https://www.future-science.com/doi/10.2144/btn-2020-0095
In Summary (Paet 2):
-there are no standardized algorithms or guidelines to ensure antibody accuracy and validity
-antibody validation remains variable in the literature and sometimes in clinical practice
-at least 50% of 2500 commercially available antibodies did not work as intended
-it is estimated that only 52% of laboratories have adopted some or all of the recommendations for IHC validation/revalidation
-reproducibility crisis in antibody research stems from end users being unaware of the need to properly validate an antibody
-even with recombinant methods, it is hard and expensive to MAKE a perfect antibody
-polyclonal antibodies represent a pool of different antibody clones
-polyclonal antibodies also represent a batch-specific mix that will ultimately be exhausted and is then IMPOSSIBLE TO REPRODUCE EXACTLY
-monoclonal antibodies directed at a target are not all devoid of their own SPECIFICITY and REPRODUCIBILITY issues
-their first step towards antibody validation is to FORM A HYPOTHESIS for the expected localization of expression of the target of interest
-application of the candidate antibody in substantially increased concentration may result in NONSPECIFIC staining patterns
-antibody reproducibility is a critical step for validation of any antibody to standardize an IHC assay, but was not mentioned as a pillar by Uhlen et al
-antibody reproducibility can sometimes be challenging to prove if the target is heterogeneously expressed in the target tissue
-many commercial vendors point out that the epitope is the ‘secret sauce’ that makes their antibody better than other competitors
-research labs in the academic sector are not subject to any certification and peer review is the only ‘regulatory body’
-the affinity and dissociation constants for most monoclonal antibodies are not known or not easily available
All of this is to say: ANTIBODIES ARE NOT SPECIFIC. Next time they try to claim that "specific" antibodies are targeting certain "viruses" or their "spike proteins," hopefully you will now know better and realize that this is never the case.
https://docs.google.com/document/d/e/2PACX-1vQbMvfH_zyuzbOFynD1PFEAdLYVCStkXeVld8PxJ6K0U7i2FMZ4hAx0qgdB2VITeTQeyAaKeeVR0YOM/pub
posts on the Reproducibility Crisis:
Science:
https://docs.google.com/document/d/e/2PACX-1vQnl8aBMGbDsNfRW1S9CH-s7bKatf9AQ_Ff9CvgqGpbiR_lcZ_zxf5tJdvDuSkvx6dUPJy5cfiJy9Ej/pub
Cell Cultures:
https://docs.google.com/document/d/e/2PACX-1vQfoMdQAMeYP0jJv6vHPPQtYleDrj1bsso67SQC3Q9iDHCjcoq1I_Yzj2vvbRaRTIUXHQjYD0HCLnoy/pub
_
More info on Antibody deception:
The Misinterpretation of the Antibodies
A closer look at antibodies is more important today than ever. After showing in my other
articles that there is no proof of the existence of a pathogenic virus, because none of the
claimed pathogenic viruses have fulfilled Koch's postulates, the "antibody" card has now
been played by the vaccination advocates. Their claim (which has been drilled into heads
for decades) that they are the indirect proof of a pathogen, or offer protection against a
pathogen X, is based on an error. This assertion has been repeatedly exposed as false.
Since being asked again and again what these antibodies are, I would like to show in this
article that antibodies are no proof of protection, nor that they work specifically as in the
key/lock theory.
What is a titer increase?
Quote: Dr. Stefan Lanka: (backup available)
"The increase is nothing more than the body's reaction to poisoning [adjuvants], when the
body is poisoned, holes are torn in the cells by these poisons and the cells are destroyed.
The body's reaction when cells break down is to form sealing substances (globulins), small
protein bodies that immediately expand in acidic environments, become flat and cross-link
with their hydrogen sulphide groups (in which energy is stored) with other proteins and
other things.
These cause blood to clot and wounds to heal and they seal our cells when toxins are
injected into the body. Even if you get a blow on a muscle, (forming a bruise) or a blow on
the kidney (especially sensitive), or the liver, there is an immediate increase in titer. The
body reacts to this by sealing the damaged cells and sealing growing cells.
It's like a house that leaks until the windows are in and sealed. They called this an
antibody and even a specific antibody, which is not true. The binding property of these
hydrogen sulfidetype proteins is non specific, they bind to all sorts of things. You can
manipulate this in the laboratory by changing the acid level, adding detergents that change
the mineral concentration to achieve a binding or not.
The blood of a pregnant woman is full of globulins to seal the placenta, which is constantly
growing, to accomodate the baby. The blood of a pregnant woman has to be diluted 40
times to avoid a massive positive result in tests, such as an HIV test."
The approval of vaccines is limited to so-called seroconversion.
All vaccines for Europe are approved by the EMA (European Medicines Agency) in
London. Their demand for proof of efficacy is limited solely to so-called seroconversion.
Seroconversion shows the formation of measurable antibodies in the blood of vaccinated
persons, which are equated to a protective effect.
However, when assessing immunity or the effectiveness of vaccinations, this decisive
limitation is again put into perspective by the fact that (almost) all current vaccinations are
developed primarily to form antibodies: "Although mucosal and cellular immune responses
are clearly important to protection by some vaccines, most vaccines licensed today
depend for their efficacy on serum antibodies.” (Plotkin 2010 [5] and 2001 [6]).This is not
least of all important for the development and approval of vaccines, as they have to prove
their efficacy in this context - which is done without exception (and in many cases
exclusively!) by determination of provoked antibodies.
Even long-standing STIKO members do not always seem to be aware of this correlation
when they question the usefulness of titres after vaccinations - after all, the proof of
efficacy of the respective vaccinations is based on the detection of precisely these
antibodies.
According to Prof. Heininger:
”For none of the generally recommended so-called basic vaccinations is a routine control
of the vaccination success planned or even advisable". (Heininger 2017) [7] or the blanket
statement regarding the measles vaccination, "that a positive laboratory result does not
certify protection" (Heininger 2016) [8] - If the latter were the case, the vaccination could
not have been certified as effective and therefore approved...
However, in medicine we have known for decades that circulating antibodies are not
synonymous with protection against a disease, a fact that can be understood even by
laypeople using short examples.
If antibodies do indicate protection, how do the following statements of the RKI, STIKO and
Arzneitelegram fit in?
1. The April 2001 telegram of medicines states: [1]
"Vaccine-induced titre increases are also unreliable substitutes for efficacy. What benefit
or harm the vaccinated person can expect cannot be deduced from such findings."
2. The RKI (Robert Koch Institute) writes: [2]
"For some vaccine-preventable diseases (e.g. pertussis) there is no reliable serological
correlate that could be used as a surrogate marker for existing immunity. Furthermore, the
antibody concentration does not allow any conclusion to be drawn about a possible
existing cellular immunity.”
3. Prof. Heininger, a long-standing member of the STIKO (permanent vaccination
commission) writes: [3]
"It is neither necessary nor useful to determine efficacy by blood sampling and antibody
determination after a vaccination has been carried out. On the one hand, even an antibody
determination does not provide a reliable statement about the presence or absence of
vaccination protection, and on the other hand, it is simply too expensive.”
4. Sick despite vaccination? [4]
An example of this was a 14-year-old boy who had received sufficient basic immunisation
in childhood and a booster against tetanus six months earlier when he developed tetanus.
Laboratory tests revealed antibodies so high that, according to the definition of antibody
titres, he should have been protected. But he was not! This example shows that the theory
of antibodies as "protective magic bullets" is wrong. The RKI then coined the term "non-
protective" antibodies.
5. Prof. Heininger - STIKO (2017) [7]
"The most important thing right from the start: For none of the generally recommended so-
called basic vaccinations is a routine control of the vaccination success planned or even
advisable".
6. Prof. Heininger - STIKO (2016) [8]
"...there are not only false-negative IgG antibody results (which would not bother us if the
child received an MMR vaccination as a consequence), but unfortunately also false-
positive results. This must be put to parents so that they understand that a positive
laboratory result does not certify protection and that they are much better advised to give
their child a second dose of MMR".
Remark: So again confirmation that a positive laboratory result is insignificant. The
question arises again and again as to how you know that antibodies offer circulating
protection when the highest authorities themselves say that a titer increase cannot prove
protection exists. When people have high antibody levels, do they still fall ill? If no one can
say exactly at what titer level there is real protection, why is the approval of a vaccine
based on that exact reading? Personally, this makes me more than a little suspicious.
The following points are of crucial importance in this discussion:
•Firstly, that we cannot always be sure that the question of immunity can be clarified
by means of an antibody determination for each vaccine (see below)
•Secondly, the antibodies that show up in routine tests are not automatically those
that provide protection (immunity), but sometimes only those that indicate that
(apart from the measured protective antibodies that are not decisive for immunity,
and which are certainly not measured) protective antibodies have been produced.
The measured ones are then a so-called surrogate parameter of immunity. This
complicated hypothesis is based, on one hand, on the fact that the immune
response produces numerous different antibodies with different functions and, on
the other hand, that the determination of the actually decisive antibodies in some
vaccinations would be too time-consuming for routine diagnostics. (Or to put it
simply, the connection between antibodies and immunity is a myth)
•Thirdly, each 'immunity' is based on statistics and therefore relative whether it
protects in the individual case or not. The true reasons for the state of the body
being "symptom-free" lie buried in other justifications. "Thus protection is a
statistical concept. When we say that a particular titer of antibodies is protective, we
mean under the usual circumstances of exposure, with an average challenge dose
and in the absence of negative host factors.” [6
•Fourthly, the question of protection from what exactly is meant from the point of
view of orthodox medicine is also crucial. For example, it is claimed that in the case
of HiB and measles, much lower antibody levels protect against contracting the disease oneself (protection from disease) than is necessary to prevent transmission to others (protection from infection). Note: As there is still no scientific proof of the measles virus, the question naturally arises as to how the claim of protection from measles by antibodies can be claimed when the pathogen has not yet been proven. A fallacy. So the horse is being put before the cart here. I'm measuring some "antibodies", so I'm indirectly claiming to have a pathogen. The measurable antibody titers after vaccination only shows the conflict of the immune system with the antigens, which are mostly coupled to adjuvants. Without these adjuvants there would be no antibody formation. Here it becomes clear that the immune system is much more complex and does not function exclusively through antibody formation. Herpes sufferers develop circulating antibodies against the herpes virus. Nevertheless, herpes can flare up again and again by weakening the immune system, for many people disgust is enough. And this occurs even when herpes antibodies are detectable. Someone who is HIV-positive is also not happy about having circulating antibodies against HIV. The hypothesis of antibodies does not work from start to finish. If they can offer protection, how is it that people who have a sufficient titer still fall ill? How is it possible that the logic of antibodies in HIV was turned 180 degrees, where high antibodies are deemed counterproductive? No antibodies are required, protection by vaccination is always assumed without evidence. The phantom is always assumed, they don't even want to think in other directions! It's not science.
...... THE REST OF THIS ARTICLE HERE
Stefan-Lanka-The-Misinterpretation-of-the-Antibodies-English-Translation.pdf (truthseeker.se) Https://truthseeker.se/wp-content/uploads/Stefan-Lanka-The-Misinterpretation-of-the-Antibodies-English-Translation.pdf
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