In the paper we read about COVID-19, the authors spent a fair bit of space discussing lymphocyte exhaustion. They suggested that one potential driver for this could be that the continued presence of antigen in chronic viral infection impair[s] the growth of memory CD8+ T cells and impair[s] the function of effective CD8+ T cells. So, to summ

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In the paper we read about COVID-19, the authors spent a fair bit of space discussing lymphocyte exhaustion. They suggested that one potential driver for this could be that the continued presence of antigen “in chronic viral infection impair[s] the growth of memory CD8+ T cells and impair[s] the function of effective CD8+ T cells.” So, to summarize, if there’s still a ton of antigen out there, Tc cells can get exhausted. Now, they never connected the following dots explicitly, but they mentioned something about early immune responses that might help explain why there is more viral antigen present, and thus more T cells exhaustion. Specifically, they wrote that the virus can reduce a host’s production of type I IFNs (we talked about these as IFN-?/?).

Explain why and how a reduction in these signaling molecules could lead to higher levels of viral antigen being present.

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