key: cord-0743721-ejjg2pex authors: Achiron, Anat; Mandel, Mathilda; Dreyer-Alster, Sapir; Harari, Gil; Gurevich, Michael title: Humoral SARS-COV-2 IgG decay within 6 months in COVID-19 healthy vaccinees: The need for a booster vaccine dose? date: 2021-10-27 journal: Eur J Intern Med DOI: 10.1016/j.ejim.2021.10.027 sha: 960cd0549ebc717b3aa290c632f09859075fb54d doc_id: 743721 cord_uid: ejjg2pex nan 95% efficacy in preventing COVID-19 disease [2] . As the process of vaccination against COVID-19 is currently spreading all over the world, it is of importance to assess the longevity of the humoral immune response to the vaccination. A high percentage of protective antibody responses was reported 7 days after full vaccination with BNT162b2 [3] . In a very recent study anti-RBD IgG was detected in 100% of fully vaccinated individuals at days 33-55 for both the Moderna and Pfizer cohorts [4] . To better understand the longevity of the humoral response, we conducted a prospective longitudinal study among a cohort of healthy vaccinees up to eight months from the second vaccine dose. subjects <60 years an inverse correlation was observed (r= -0.502). No significant differences were observed in the decay kinetics in relation with gender. Our findings demonstrate that anti-S1 IgG levels determined across 1 to 8 months after full vaccination, waned with an estimated half-life of 45 days. Age was associated with lower post-vaccination anti-S1 IgG titers and with accelerated IgG decrease over time. Moreover, we calculated that within 225 days (5*t 1/2 ), IgG will decrease below detection level, raising the need for reconsidering the current mRNA vaccine regiments. In comparison, seasonal coronavirus protective immunity in convalescents was reported to be similarly short-lasting up to one year [5] . However, for SARS-CoV and MERS, IgG antibodies remained detectable in 100% and 74.2% of subjects respectively, for 1-3 years post-infection [6] . Our group recently reported that 85% of convalescent COVID-19 subjects had a protective IgG level that prevailed over a period of up to 9 months post-infection, regardless of age or gender [7] . The question of long-lasting and protective vaccine immunity against SARS-CoV-2 is of major importance as the decay suggests the need for an additional booster. A decrease in IgG levels impairs the equilibrium between COVID-19 viral load during exposure and humoral protection. The induction and decay of antigen-specific IgG response to COVID-19 mRNA vaccine are consistent with the known serum T½ of various IgG subclasses immunoglobulin [8] . Among fully vaccinated health care workers, the occurrence of SARS-CoV-2 infection correlated with lower neutralizing antibody titers during the peri-infection period [9] . Older vaccinees, aged ≥ 60 years, demonstrated a more profound BNT162b vaccines are immunogenic and protect non-human primates against SARS-CoV-2. bioRxiv Safety and efficacy of the BNT162b2 mRNA Covid-19 vaccine Antibody responses to SARS-CoV-2 vaccines in 45,965 adults from the general population of the United Kingdom Evolution of Anti-SARS-CoV-2 IgG Antibody and IgG Avidity Post Pfizer and Moderna mRNA Vaccinations Seasonal coronavirus protective immunity is short-lasting A systematic review of antibody mediated immunity to coronaviruses: kinetics, correlates of protection, and association with severity SARS-CoV-2 antibody dynamics and B-cell memory response over time in COVID-19 convalescent subjects The half-lives of IgG subclasses and specific antibodies in patients with primary immunodeficiency who are receiving intravenously administered immunoglobulin Covid-19 breakthrough infections in vaccinated health care workers Paired circulating antibodies to SARS-CoV-2 over time in healthy vaccinated subjects. Longitudinal spike IgG (n=39, BAU/ml Subjects aged >60 years are depicted in blue, subjects aged ≤ 60 years in red Author Contributions All authors had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Drs Achiron and Mandel contributed equally to this work Acquisition, analysis, or interpretation of data: All authors Drafting of the manuscript: All authors Critical revision of the manuscript for important intellectual content: All authors. Statistical analysis: Dr Harari. Obtained funding: Dr Achiron. Supervision: Dr Achiron. Declaration of Competing Interest Anat Achiron BSc -no conflicts of interest PhD -no conflicts of interest Michael Gurevich -no conflicts of interest Funding/Support This work was funded by research grants from the Sheba Medical Center (GN. 04027-10/1001493), and the Laura Schwarz-Kipp Research Fund for Autoimmune Diseases (GN. 0601253231)