The researchers observed these changes as much as a year after the participants came down with COVID-19. Due to the small number of study participants, the scientists could not establish a direct association between the cellular and molecular changes and health outcomes.
The investigators suspected that an inflammatory cytokine called IL-6 might play role in establishing the changes in gene-expression instructions. They tested their hypothesis both in mice with COVID-19-like disease and in people with COVID-19. In these experiments, some of the subjects received antibodies at the early stage of illness that prevented IL-6 from binding to cells. During recovery, these mice and people had lower levels of altered stem cell gene-expression instructions, monocyte production and inflammatory cytokine production than subjects that didn't receive the antibody. In addition, the lungs and brains of mice that received the antibodies had fewer monocyte-derived cells and less organ damage.
Additionally, the findings suggest that early-acting IL-6 is likely a major driver of long-term inflammation in people with severe COVID-19. These findings shed light on the pathogenesis of SARS-CoV-2 infection and may provide new leads for therapies. The results also underscore the importance of staying up to date with recommended COVID-19 vaccines, which are proven to protect against serious illness, hospitalization and death.
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