COVID vaccines may impair long-term immunity to the virus

Research suggests that vaccination against COVID via mRNA vaccines may reduce body’s ability to produce key type of antibody.

Vaccines against the coronavirus may impair the body’s ability to produce a key type of antibody, thus potentially limiting the immune system’s defenses against mutated strains of the virus, a new study suggests.

The study draws upon data collected during Moderna’s randomized control trial for its mRNA SARS-CoV-2 vaccine, from July 2020 through March 2021.

Researchers looked at participants who tested positive for the coronavirus during the trial, comparing serum levels of specific types of antibodies, based on vaccination status, as well as viral load.

In particular, the study looks at the antibody response to the virus’ nucleocapsid protein core, using the anti-nucleocapsid antibodies levels (anti-N Abs) as a marker for comprehensive immune system response to the virus, as opposed to the narrower response to the spike protein. Variants of SARS-CoV-2 with mutated spike proteins have been a subject of concern for the reliance of vaccinated immunity on antibodies targeting the s-proteins of the original variant.

As expected, serum levels of the anti-nucleocapsid antibodies varied based on measured viral load in both the placebo and vaccine cohorts, with participants who had higher viral loads found to have higher levels of neutralizing anti-nucleocapsid antibodies.

Researchers also found a pronounced difference, however, in the levels of anti-nucleocapsid antibodies between vaccinated participants and members of the placebo cohort, even when the study controlled for viral load.

Trial participants who were given the placebo, rather than the vaccine, and became infected during the trial were found to have significantly higher levels of the neutralizing anti-nucleocapsid antibodies than vaccinated participants who had comparable viral loads.

Approximately 60% of participants from the placebo cohort who experienced very mild infection, with low viral loads, were found to have anti-nucleocapsid antibodies, compared to roughly 10% of vaccinated subjects.

Among those with higher viral loads – qualifying as mild cases, rather than very mild – 71% of the unvaccinated developed anti-nucleocapsid antibodies, compared to just 15% of those in the vaccine group.

Of all unvaccinated subjects who had been diagnosed with the virus during the trial, nearly all (93%) had measurable levels of anti-nucleocapsid antibodies, compared to less than half (40%) of those in the vaccine cohort.

“While an increase in seroreversion cannot be ruled out, given the short time frame the more likely explanation is a vaccine-induced reduction in seroconversion,” researchers wrote, suggesting that trial participants given the vaccine had reduced levels of the anti-nucleocapsid antibodies as a direct result of the vaccine’s narrow focus on the spike protein.

The researchers also hinted that the diminished anti-nucleocapsid antibody response among the vaccinated could lead to undercounting of breakthrough cases, when measured by antibody sampling.

“Even with frequent serosampling, serosurveys that rely on antibodies to the N protein may underestimate within-community transmission dynamics.”