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Covid-19 Part 1: Antibody-dependent Enhancement of Disease

Covid-19 Part 1: Antibody-dependent Enhancement of Disease
Jan 6, 2023 · 33m 34s

The severity of COVID-19 varies by individual spanning from asymptomatic, mild, moderate, severe, critical, and chronic disease. Prior to the availability of vaccines, high antibody titers correlated with disease severity....

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The severity of COVID-19 varies by individual spanning from asymptomatic, mild, moderate, severe, critical, and chronic disease. Prior to the availability of vaccines, high antibody titers correlated with disease severity. This was also observed for SARS disease. These high antibody titers on initial infections result from memory B cell responses with cross-reactive antibody responses from previous infection of likely other betacoronavirus family members. In general, family members of the betacoronavirus family leverage Fc receptor antibody uptake of viruses by phagocytic cells to infect these innate immune cells. This extended cellular tropism of phagocytic immune cells is dependent upon Fc receptors and antibodies. It is hypothesized that SARS-CoV-2 with higher antibody titers can infect phagocytic immune cells; SARS-CoV-2 infection of these cells has been observed in some patients with severe COVID-19. This proposed antibody-dependent enhancement (ADE) of disease has been proposed to a key transition of infection from respiratory infection to multi-organ disease in some severe COVID-19 patients. While the main medical community believes that there is no ADE associated with SARS-CoV-2 infections, multiple clinical studies are consistent with SARS-CoV-2 infection of monocytes and macrophages in some severe COVID-19 patients. The podcast discusses data available in the summer of 2022.
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