Antibody Responses After Sars Cov 2 Infection

Antibodies develop shortly after exposure to an antigen as part of the adaptive immune response. In the acute phase of infection, antibodies respond by neutralization, opsonization of antigens, and stimulation of other immune system components. In the convalescent phase, antibodies persist despite antigen clearance, thanks to plasma cells. Upon antigen re-exposure, activated memory cells rapidly differentiate into plasma cells and contribute high affinity antibodies. In January of 2020, Severe Acute Respiratory Syndrome Coronavirus Two (SARS- CoV-2), a novel coronavirus, was identified, and a pandemic was declared a couple of months later. Severity of coronavirus disease 2019 (COVID-19) ranged from asymptomatic disease to respiratory failure leading to hospitalization, intubation, and death. Little was known about the immune response to SARS-CoV-2, given its recent emergence in humans and rapid spread. Here I investigate antibody responses after SARS-CoV-2 infection, specifically investigating anti-viral antibody responses in the early and late convalescent periods. I find that in the early convalescent period, anti-viral antibodies are elevated, including neutralizing antibodies. And higher anti-viral antibody levels are associated with more severe COVID-19, older age, male sex, higher body mass index, and symptoms, including fever and low appetite. In the late convalescent period, I find that some anti-viral antibodies persist for a year while others decline. I determine that anti-membrane antibodies in combination with anti-spike antibodies can be used to differentiate past SARS-CoV-2 infection and vaccination, and that both anti-membrane and anti-spike antibodies persist for at least one year, in contrast to the anti-nucleocapsid antibodies that decline over several months. I also investigate autoantibodies detected after SARS-CoV-2 infection. Little was known about rheumatoid factors, antibodies that bind to the Fc region of IgG, after recent infection. I find that rheumatoid factors after COVID-19 bind to unique, novel linear epitopes in the CH2 and CH3 regions of IgG Fc and bind viral antigens, including the SARS-CoV-2 spike protein. Taken together, these findings contribute to our knowledge of the antibody response following SARS-CoV-2 infection and highlight the potential contributions of antibodies that recognize foreign and self-antigens, linking infectious disease and autoimmunity.