Anti-SARS-CoV-2 IgG Antibody Response in Individuals Infected Post Complete Vaccination: A 6-Month Longitudinal Study in Healthcare Professionals

Abstract

Serological assays have been used to evaluate the magnitude of naturally acquired and BNT162b2 vaccine-induced immunity. In order to assess the extent to which the antibody response correlates with infection-mediated protection after vaccination, we investigated the kinetics of anti-SARS-CoV-2-S1 IgG in fully vaccinated healthy individuals who did or did not develop COVID-19 within 8 months after the booster dose. The anti-SARS-CoV-2-S1 receptor-binding, domain-specific IgG titer was assessed in serum samples collected at various intervals from 4 months after the second and 6 months after the third dose. The IgG level decreased 33% within 6 months after the second dose and, one month after the third dose, increased dramatically (>300%) compared with the pre-booster time point. COVID-19 infection within two months after the third dose did not cause significant IgG variation, but later viral infections elicited an IgG response similar to the initial response to the booster. The probability of developing COVID-19 and the severity of symptoms were not related to the antibody titer. Our data indicate that repeated exposure to viral antigens by either vaccination or infection at short-term intervals elicits limited boosting effects and that an IgG titer alone is not associated with the prediction of future infections and their symptomatology.

Long-Term Analyses of SARS-CoV-2 Humoral and T Cell Responses and Breakthrough SARS-CoV-2 Infections after Two Doses of BNT162b2 Followed by mRNA-1273 and Bivalent Omicron-Adapted BNT162b2 Vaccines: A Prospective Study over 2 Years in Non-Immunocompromised Individuals

“…The first phase, spanning the first 9 months after the second dose of BNT162b2, was characterized by a progressive decrease in anti-RBD antibodies. As observed in other studies, anti-RBD antibody titers were higher at all time points in subjects previously infected with an ancestral SARS-CoV-2 variant [ 12 , 13 , 14 , 15 , 16 ]. The few breakthrough infections that occurred in this phase were most likely the consequence of waning of vaccine-induced protection and the dominance of the Delta (B.1.167.2) variant, with its increased replicating fitness and evasiveness from BNT162b2-induced neutralizing antibodies [ 17 , 18 ].…”