Corona Cross-Reactivity

According to the mainstream narrative, “antibodies” are proteins that react to antigens—substances identified as foreign, such as toxins, proteins, peptides, or polysaccharides

The prevailing pseudoscientific hypothesis claims that each “antibody” binds to a specific antigen, like a lock and key.

In the case of “SARS-COV-2,” “antibodies” said to be specific to the spike protein are believed to form either after “infection” with the “virus” or through vaccination, which allegedly programs the body to produce the spike protein via mRNA instructions.

Once enough “antibodies” accumulate, they are said to be detectable through “antibody” tests.

However, detection is claimed to occur only after an “infection” has run its course, since the body is thought to take time to generate an “antibody” response.

Unlike HIV, where “antibody” tests supposedly indicate an active “infection,” we are told that “Covid antibody” tests (and those for other “viruses”) serve only to determine past exposure and assess whether an individual has developed some degree of “immunity.”

“Antibody tests should not be used to diagnose a current infection with the virus that causes COVID-19.

An antibody test may not show if you have a current infection, because it can take 1 to 3 weeks after the infection for your body to make antibodies.”

https://www.cdc.gov/coronavirus/2019-ncov/symptoms-testing/testing.html

In order for “antibody” test results to have any sort of meaing, specificity—refering to an “antibody’s” ability to recognize and bind exclusively to a single, unique antigen—is absolutely essential.

Many assume these tests are highly accurate and specific, but the reality is far more complicated. While marketed as detecting specific “antibodies,” cross-reactivity—where “antibodies” bind to unintended antigens—is a well-documented issue.

This undermines claims of specificity, making test results questionable at best. Although such limitations are rarely emphasized, even the CDC acknowledges them in its own reports.

Antibody Testing Guidelines

“Testing for antibodies that indicate prior infection could be a useful public health tool as vaccination programs are implemented, provided the antibody tests are adequately validated to detect antibodies to specific proteins (or antigens).

Although an antibody test can employ specific antigens, antibodies developed in response to different proteins might cross-react (i.e., the tests might detect antibodies they are not intended to detect), and therefore, might not provide sufficient information on the presence of antigen-specific antibodies.

For antibody tests with FDA EUA, it has not been established whether the antigens employed by the test specifically detect only antibodies against those antigens and not other antigens.

https://www.cdc.gov/coronavirus/2019-ncov/lab/resources/antibody-tests-guidelines.html

The CDC explicitly states that no FDA EUA-approved “SARS-COV-2 antibody” test has been definitively established to detect only “antibodies” specific to “SARS-COV-2” antigens.

This raises serious concerns about the validity of these tests, as cross-reactivity with “antibodies” from other “infections” would lead to misleading results.

This issue becomes even more apparent when considering that there are no properly purified and isolated “viruses” to serve as definitive standards for “antibody” test calibration—just as there are no directly isolated “antibodies” proven to be specific to “SARS-COV-2.”

Making matters worse, PCR—an already problematic test—is routinely used to confirm “positive” samples in “antibody” test validation studies. This means that one unvalidated, inherently flawed test is being used as the benchmark for another unvalidated, inherently flawed test, creating a fraudulent circular validation process that lacks independent confirmation of accuracy.

EUA Authorized Serology Test Performance

“The performance of these tests is described by their “sensitivity,” or their ability to identify those with antibodies to SARS-CoV-2 (true positive rate), and their “specificity,” or their ability to identify those without antibodies to SARS-CoV-2 (true negative rate). A test’s sensitivity can be estimated by determining whether or not it is able to detect antibodies in blood samples from patients who have been confirmed to have COVID-19 with a nucleic acid amplification test, or NAAT.

In some validation studies of these tests, like the one the FDA is conducting in partnership with the National Institutes of Health (NIH), the Centers for Disease Control and Prevention (CDC), and the Biomedical Advanced Research and Development Authority (BARDA), the samples used, in addition to coming from patients confirmed to have COVID-19 by a NAAT, may also be confirmed to have antibodies present using other serology tests.

A test’s specificity can be estimated by testing large numbers of samples collected and frozen before SARS-CoV-2 is known to have circulated to demonstrate that the test does not produce positive results in response to the presence of other causes of a respiratory infection, such as other coronaviruses.

These estimates of sensitivity and specificity are just that: estimates. They include 95 percent confidence intervals, which are the range of estimates we are about 95 percent sure a test’s sensitivity and specificity will fall within given how many samples were used in the performance validation. The more samples used to validate a test, the smaller the confidence interval becomes, meaning that we can be more confident in the estimates of sensitivity and specificity provided.

Tests are also described by their Positive and Negative Predictive values (PPV and NPV). These measures are calculated using a test’s sensitivity, its specificity, and using an assumption about the percentage of individuals in the population who have antibodies to SARS-CoV-2 (which is called “prevalence” in these calculations). Every test returns some false positive and false negative results.

The PPV and NPV help those who are interpreting these tests understand, given how prevalent individuals with antibodies are in a population, how likely it is that a person who receives a positive result from a test truly does have antibodies to SARS-CoV-2 and how likely it is that a person who receives a negative result from a test truly does not have antibodies to SARS-CoV-2.

The PPV and NPV of a test depend heavily on the prevalence of what that test is intended to detect. Because all tests will return some false positive and some false negative results, including tests that detect antibodies to SARS-CoV-2, broad use of the tests, when not appropriately informed by other relevant information, such as clinical history or diagnostic test results, could identify too many false-positive individuals.”

https://www.fda.gov/medical-devices/coronavirus-disease-2019-covid-19-emergency-use-authorizations-medical-devices/eua-authorized-serology-test-performance

On top of these issues, there is no established correlation between “antibody” levels and “protection” from “infection” or disease, referred to as the correlation of protection. In other words, there is no defined threshold for how many “antibodies,” if any, are needed to prevent illness.

Without a clear link between “antibody” presence and “immunity,” these tests fail to provide meaningful or actionable information. Ultimately, this calls into question the entire premise on which “antibody” testing is based, making the results from these tests meaningless.

The Flawed Science of Antibody Testing for SARS-CoV-2 Immunity

“The early consumer tests’ accuracy was unproven, making the results somewhat dubious. More fundamentally, the so-called correlates of protection were unknown. Which specific antibodies guarded against SARS-CoV-2 reinfection? How high did their levels need to be? And how long would they provide a reliable defense?”

“Therefore, the agency in its May 19 communication stated that “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.”

“The problem isn’t simply that the tests weren’t designed to assess immunity, experts told JAMA. It’s also that the protective antibodies and their thresholds still haven’t been fully worked out.”

https://jamanetwork.com/journals/jama/fullarticle/2785530

Specificity in testing is crucial because, without high specificity, an “antibody” test cannot reliably determine whether someone was exposed to “SARS-COV-2” or to an entirely different antigen.

If an “antibody” reacts to multiple, unrelated proteins, then a positive test result does not confirm prior “infection” with “SARS-COV-2,” or any other “virus” for that matter. A lack of specificity renders these tests unreliable for both individual diagnosis and public health policy.

Furthermore, this issue extends beyond testing—it directly contradicts the narrative that vaccines produce highly specific “immune” responses. If “SARS-COV-2 antibodies” can bind to multiple antigens, then how can it be claimed that vaccines induce “immunity” against a specific “virus?”

If these same “antibodies” are present due to exposure to other antigens, then a vaccine-induced “immune” response cannot be distinguished from natural exposure to unrelated substances or “pathogens.”

This should raise serious doubts about the claimed effectiveness of these injections and whether any measured “antibody” response is truly protective or merely a generic reaction that has been misinterpreted.

This lack of specificity of “antibodies” is not theoretical—it is well-documented in the “scientific” literature. Numerous studies have reported cross-reactivity in “SARS-COV-2 antibody” tests, where “antibodies” claimed to be specific to the “virus” also bind to antigens from many other sources.

As specificity is an essential tenet of “antibody” research and the prevailing “immunity” narrative, let’s examine these studies and find out exactly how nonspecific these “antibodies” truly are.

We begin this examination with a study published in June 2020 which highlighted the importance of understanding cross-reactivity, stating that it is crucial for properly interpreting serologic tests, such as serosurveys and clinical “antibody” tests.

To gain a better understanding of this, the researchers evaluated serologic reactivity using pre-2019 archival blood serum samples (“pre-pandemic”) and samples from a community highly affected by “SARS-COV-2” in April 2020.

In other words, half of the blood and serum samples tested came from before “SARS-COV-2” supposedly existed. The researchers tested IgG, IgM, and IgA reactivity against spike proteins from “SARS-COV-2,” “MERS,” “SARS-COV-1,” “OC43,” and “HKU1” using twelve previously reported ELISAs.

Their results showed that “antibodies” supposedly specific to “SARS-COV-2” also reacted with “MERS” and “SARS-COV-1,” revealing a lack of specificity to the intended “viral” target.

The researchers tried to explain away this cross-reactivity by suggesting that individuals who strongly seroconverted after “SARS-COV-2 infection” could have “antibodies” that are universally reactive to multiple “Betacoronaviruses,” including “MERS” and “SARS-COV-1.”

They also cautioned that in regions with higher prevalence of “MERS” and “SARS-COV-1,” archival sera should be considered to adjust estimates of seropositivity, highlighting the potential issue of misinterpreting “antibody” results due to cross-reactivity.

Despite the excuses presented, the evidence clearly showed that the so-called specific “antibodies” to “SARS-COV-2” were binding to its relatives.

Serologic cross-reactivity of SARS-CoV-2 with endemic and seasonal Betacoronaviruses

“Furthermore, knowledge of cross-reactivity is necessary to understand and properly interpret results from serologic studies such as serosurveys and clinical antibody tests (13, 14).

Previous research has shown minimal cross-reactivity between RBD domains from differing coronaviruses; however, these studies largely ignore the rest of the spike protein, which will be an important consideration for identification of potential therapeutic antibodies and can be used in vitro to help identify polyclonal responses that are not detected with RBD alone (15).

Here, we evaluated the serologic reactivity of pre-pandemic archival blood serum samples (pre-2019) and samples collected in April 2020 from a community highly affected by SARS-CoV-2. Utilizing twelve previously reported ELISAs (15), we tested IgG, IgM and IgA reactivity against spike proteins from SARS-CoV-2, MERS-CoV, SARS-CoV, HCoV-OC43, and HCoV-HKU1 (Fig. 1).”

“When comparing serum from healthy volunteers collected pre-2019 (archival controls) to those from a high-exposure community, we observe that SARS-CoV-2 antibodies react intermediately with MERS and SARS-CoV spike proteins. The mean ELISA signal intensity is significantly greater for both MERS and SARS-CoV when comparing archival controls versus the high-incidence community.”

“Given the low seroprevalence of SARS-CoV and MERS outside of their endemic regions, and the significantly lower reactivity of SARS-CoV-2 patient sera to SARS-CoV and MERS spike proteins, it is likely that any reactivity between the pandemic SARS-CoV-2 pandemic and MERS/SARS-CoV endemic viruses would result in minimal noise between SARS-CoV-2 signal and endemic coronavirus signal in serological assays.

In countries with a higher prevalence of MERS & SARS-CoV, researchers should include thorough analysis of archival patient sera (pre-2019), including sera from known SARS-CoV and MERS convalescent patients, to properly analyze the resulting data and adjust any estimates of seropositivity as needed. No clinical serology studies of SARS-CoV-2 immunity in populations previously infected with either SARS or MERS have yet emerged.

Additionally, individuals who have strongly seroconverted after SARS-CoV-2 infection, and who display cross-reactivity for both MERS and SARS-CoV spike proteins, are of great interest for translational study.

These individuals could potentially harbor antibodies that are universally reactive to multiple Betacoronaviruses and, if these antibodies are functional for neutralization, could be important to identify to inform the development of novel therapeutics or vaccines.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7315998/

In August 2020, a study found that dengue “antibody” tests also show cross-reactivity with “SARS-COV-2 antibodies.” The researchers detected 12 positive dengue cases (21.8%) out of 55 “COVID-19” patients using the dengue lateral-flow rapid test.

Additionally, 95 dengue patient samples from before September 2019 showed that 22 percent (21 out of 95) tested positive or equivocal for “SARS-COV-2” serology targeting the spike (S) protein, compared to just four percent (4 out of 102) in controls (P = 1.6E−4).

This study supported the idea of cross-reactivity between “dengue virus” and “SARS-COV-2,” which the researchers warned could lead to “false positives” in both dengue and “COVID-19” tests.

The fact that cross-reactivity was observed — with dengue” antibody” tests showing false positives in “Covid” patients and “SARS-COV-2 antibody” tests showing positives in “pre-pandemic” dengue patients — highlights the lack of specificity in both tests.

Potential Antigenic Cross-reactivity Between Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and Dengue Viruses

Results

Using the dengue lateral-flow rapid test we detected 12 positive cases out of the 55 (21.8%) COVID-19 patients versus zero positive cases in a control group of 70 healthy individuals (P = 2.5E−5). This includes 9 cases of positive immunoglobulin M (IgM), 2 cases of positive immunoglobulin G (IgG), and 1 case of positive IgM as well as IgG antibodies.

ELISA testing for dengue was positive in 2 additional subjects using envelope protein directed antibodies. Out of 95 samples obtained from patients diagnosed with dengue before September 2019, SARS-CoV-2 serology targeting the S protein was positive/equivocal in 21 (22%) (16 IgA, 5 IgG) versus 4 positives/equivocal in 102 controls (4%) (P = 1.6E−4).

Subsequent in-silico analysis revealed possible similarities between SARS-CoV-2 epitopes in the HR2 domain of the spike protein and the dengue envelope protein.

Conclusions

Our findings support possible cross-reactivity between dengue virus and SARS-CoV-2, which can lead to false-positive dengue serology among COVID-19 patients and vice versa. This can have serious consequences for both patient care and public health.

https://academic.oup.com/cid/article/73/7/e2444/5892809

In November 2020, researchers at the Francis Crick Institute and University College London “accidentally” discovered that some individuals who were never diagnosed with “SARS-COV-2” had “antibodies” that cross-reacted with the “virus” and other “coronaviruses” associated with the common cold.

To confirm their findings, they analyzed over 300 blood samples from 2011 to 2018. While most samples contained “antibodies” to common cold “coronaviruses,” a subset also showed cross-reactivity with “SARS-COV-2.”

This was found in 5.3 percent of adults, 10 percent of pregnant women, and 44 percent of children—especially those aged 6 to 16.

This is taken from a long document, see the rest here substack.com

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