Review
Immunopathology of Hyperinflammation in COVID-19

https://doi.org/10.1016/j.ajpath.2020.08.009Get rights and content
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The rapid spread of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome–coronavirus 2 (SARS-CoV-2), has resulted in an unprecedented public health crisis worldwide. Recent studies indicate that a hyperinflammatory syndrome induced by SARS-CoV-2 contributes to disease severity and mortality in COVID-19. In this review, an overview of the pathophysiology underlying the hyperinflammatory syndrome in severe COVID-19 is provided. The current evidence suggests that the hyperinflammatory syndrome results from a dysregulated host innate immune response. The gross and microscopic pathologic findings as well as the alterations in the cytokine milieu, macrophages/monocytes, natural killer cells, T cells, and neutrophils in severe COVID-19 are summarized. The data highlighted include the potential therapeutic approaches undergoing investigation to modulate the immune response and abrogate lung injury in severe COVID-19.

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Supported by NIH grant K22CA230315 (D.J.) and a Ralph Edwards Career Developmental Professorship (D.J.).

Disclosures: None declared.