Abstract
BackgroundMost studies on immune response after coronavirus disease 2019 (COVID-19) vaccination focused on serum IgG antibodies and cell-mediated immunity, discounting the role of anti-SARS-CoV-2 neutralizing IgA antibodies in preventing viral infection. This study was aimed to quantify serum IgG and IgA neutralizing antibodies after mRNA COVID-19 vaccination in baseline SARS-CoV-2 seronegative healthcare workers.MethodsThe study population consisted of 181 SARSCoV-2 seronegative healthcare workers (median age 42 years, 59.7% women), receiving two doses of Pfizer COVID-19 vaccine BNT162b2 (Comirnaty). Serum samples were collected before receiving the first vaccine dose, 21 days (before the second vaccine dose) and 50 days afterwards. We then measured anti-spike trimeric IgG (Liaison XL, DiaSorin), anti-spike receptor binding domain (RBD) IgG (Access 2, Beckman Coulter) and anti-spike S1 subunit IgA (ELISA, Euroimmun). Results were presented as median and interquartile range (IQR).ResultsVaccine administration elicited all anti-SARS-CoV2 antibodies measured. Thirty days after the second vaccine dose, 100% positivization occurred for anti-spike trimeric IgG and anti-spike RBD IgG, whilst 1.7% subjects remained anti-spike S1 IgA negative. The overall increase of antibodies level ratio over baseline after the second vaccine dose was 576.1 (IQR, 360.7-867.8) for anti-spike trimeric IgG, 1426.0 (IQR, 742.0-2698.6) for anti-spike RBD IgG, and 20.2 (IQR, 12.5-32.1) for anti-spike S1 IgA. Significant inverse association was found between age and overall increase of anti-spike trimeric IgG (r=-0.24; p=0.001) and anti-spike S1 IgA (r=-0.16; p=0.028), but not with anti-spike RBD IgG (r=-0.05; p=0.497).ConclusionsmRNA COVID-19 vaccination elicits sustained serum levels of anti-spike trimeric IgG and anti-spike RBD IgG, while also modestly but significantly increasing those of anti-spike S1 IgA.
Highlights
After the first case of severe acute respiratory syndrome coronavirus disease 2019 (SARS-CoV-2) infection has been described in the Chinese city of Wuhan, at the end of the 2019 [1], the severe and multifaceted infectious disease caused by this novel coronavirus spread across the world, achieving pandemic dimensions
Our study population consisted of a cohort of SARS-CoV-2 seronegative healthcare workers of the Pederzoli Hospital of Peschiera del Garda (Verona, Italy), who voluntary accepted to be vaccinated with the mRNA-LNPs COVID-19 vaccine BNT162b2 (Comirnaty; Pfizer-BioNTech, NY, USA)
Such percentages increased to 100% for both antispike trimeric IgG and anti-spike receptor binding domain (RBD) IgG 30 days after the second vaccine dose, whilst 1.7% of subjects remained anti-spike S1 IgA negative
Summary
After the first case of severe acute respiratory syndrome coronavirus disease 2019 (SARS-CoV-2) infection has been described in the Chinese city of Wuhan, at the end of the 2019 [1], the severe and multifaceted infectious disease caused by this novel coronavirus spread across the world, achieving pandemic dimensions. SARS-CoV-2 mainly spreads with two different mechanisms, encompassing airborne transmission through inhalation of infected droplets or aerosols, as well as by direct contact with infected objects or surfaces followed by transportation of viable viral particles to eyes, nose or mouth, where they penetrate the host cells through biding to its natural receptor, the angiotensin converting enzyme 2 (ACE-2) [2]. According to these paradigmatic modes of transmission, many mitigation measures have been endorsed to prevent or limit the risk of SARS-CoV-2 contagion, such as face covering, hand hygiene, social distancing, contact tracing and quarantine [3]. Vaccine administration uses the host natural defenses (i.e., the immune system) for developing resistance against a specific microorganism though development of three principal mechanisms, i.e., production of specific antibodies (humoral immunity), training of immune cells to produce immune mediators, to kill the pathogen and/or the infected host cells (cellular immunity), as well as forming the so-called memory cells, which could be effective to contrast recurrent or repeated infections caused by the same pathogen
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
