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A confusion of pathways: Discerning cell death mechanisms in SARS-CoV-2 infection

Lok-Yin Roy Wong1,2, Stanley Perlman3,4

  • 1Center for Virus-Host-Innate Immunity, Rutgers New Jersey Medical School, Newark, NJ 07103, USA.

Science Immunology
|July 12, 2024
PubMed

Insights

SARS-CoV-2 infection triggers cell death in infected cells via necroptosis. Uninfected cells experience delayed apoptosis and pyroptosis, explaining widespread tissue damage during severe acute respiratory syndrome coronavirus 2 infection.

Area of Science:

  • Cellular biology
  • Immunology
  • Virology

Background:

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes significant cellular damage.
  • The precise mechanisms driving injury in both infected and uninfected cells remain incompletely understood.

Purpose of the Study:

  • To elucidate the distinct cell death pathways activated in SARS-CoV-2 infected versus bystander cells.
  • To correlate specific cell death mechanisms with the observed tissue injury patterns.

Main Methods:

  • Analysis of cell death markers in lung tissue samples from SARS-CoV-2 infected individuals.
  • In vitro experiments using cell cultures infected with SARS-CoV-2.
  • Microscopic examination and molecular assays to identify necroptosis, apoptosis, and pyroptosis.

Main Results:

  • Infected cells predominantly undergo necroptosis.
  • Uninfected, bystander cells exhibit delayed apoptosis and pyroptosis.
  • These distinct cell death pathways correlate with the extent of tissue damage observed.

Conclusions:

  • SARS-CoV-2 infection induces differential cell death responses.
  • Necroptosis in infected cells and delayed apoptosis/pyroptosis in bystander cells contribute to severe COVID-19 pathology.
  • Targeting these specific cell death pathways may offer therapeutic strategies.

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