COVID-19, the most notorious infection in recent history, has been the main focus of the research community. One area of particular interest is our bodies’ immune response against COVID-19. This immune response is highly varied between patients – some are asymptomatic while others are left in critical condition. People are also interested in whether being infected with this strain of coronavirus allows you to develop antibodies that prevent a second infection. Recent research has been focused on trying to answer some of these pressing questions.
Like any other viral infection, COVID-19 elicits an immune system response. The innate immune system is the first line of defense, and then the more specific adaptive immunity slowly kicks in. B cells produce antibodies that are specific to the viral antigen, effectively marking it to be blocked from entering host cells. Helper T cells and cytotoxic T cells play the main role in destroying the virus along with viral-infected cells. Antibodies generated by B cells can recognize the same viral antigen in the future, protecting from reinfection.1
A study conducted by Seow et al. followed 65 patients and 31 healthcare workers who were either PCR-confirmed or seropositive with SARS-CoV-2. These subjects exhibited symptoms ranging from asymptomatic to critical. Researchers of this study tested the patients for antibody responses up to 94 days after symptoms were first exhibited. Results showed that in more than 95% of patients, neutralizing antibodies were detected eight days after symptoms began. Specifically, IgA and IgM antibodies declined and returned to baseline levels by 60 days, while IgG levels remained high in the majority of patients. Individuals with more severe symptoms had samples with higher antibody counts.2 Another study with 500 patients displayed similar results. In this larger sample, 90% of COVID-19 positive patients possessed antibodies from 40 days to seven months after the onset of symptoms. During the first three weeks of infection, antibody levels increased drastically. It also showed declining levels of IgA and IgM, while IgG levels remained detectable for at least six months after infection.3
New studies shed light on a phenomenon called the “cytokine storm,” during which some patients’ overly aggressive inflammatory response to the virus can cause significant damage to the body. Inflammatory responses normally produce cytokines, which prompt a variety of immune cells, including macrophages, neutrophils, and T cells to travel to the site of infection. However, during a cytokine storm, the immune system overproduces and is unable to stop producing cytokines. Abnormally high levels of cytokines cause an influx of immune cells such as cytotoxic T cells, which can release toxins that may damage vulnerable tissues and organs. Some patients with SARS-CoV-2 infection have immune systems that overreact and cause a cytokine storm, leading to lung injury and organ failure.4
The road to fully understanding COVID-19’s mechanisms and effects on our immune system is not yet complete, but researchers have been able to gain significantly greater insight since the pandemic began. While the mentioned studies on antibodies show promising results, they do not indicate full protection from reinfection. COVID-19 will still present great public health challenges in the foreseeable future.