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Subversion of Programed Cell Death by Poxviruses.

Heather S Koehler1, Bertram L Jacobs2

  • 1Department of Microbiology and Immunology, Emory University School of Medicine, Emory Vaccine Center, Atlanta, GA, 30322, USA.

Current Topics in Microbiology and Immunology
|January 28, 2021
PubMed
Summary
This summary is machine-generated.

Poxviruses inhibit programmed cell death, including necroptosis, using multiple strategies. Some block host sensing pathways, while others mimic host proteins to disable cell death executioners, highlighting an evolutionary arms race.

Keywords:
ApoptosisE3LInterferonNecroptosisPoxvirusesProgramed cell deathZ-nucleic acid-binding protein

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Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Poxviruses are known inhibitors of apoptosis.
  • Recent studies reveal poxviruses also inhibit necroptosis via distinct mechanisms.
  • Necroptosis is a programmed form of inflammatory cell death crucial in host defense.

Purpose of the Study:

  • To elucidate the strategies employed by poxviruses to inhibit necroptotic cell death.
  • To understand the evolutionary significance of viral inhibition of programmed cell death.

Main Methods:

  • Analysis of poxvirus interactions with host necroptosis signaling pathways.
  • Investigating viral protein functions in blocking Z-DNA binding protein 1 (ZBP1) and receptor-interacting protein kinase 3 (RIPK3) signaling.
  • Examining viral MLKL (mixed lineage kinase-like protein) mimics.

Main Results:

  • Vaccinia virus E3 protein inhibits ZBP1-mediated necroptosis but not TNF or TLR3-induced necroptosis.
  • Other chordopoxviruses utilize viral MLKL mimics to inhibit all necroptosis pathways.
  • Poxviruses employ diverse strategies to block host necroptosis.

Conclusions:

  • Poxviruses have evolved multiple, sometimes redundant, mechanisms to inhibit programmed cell death.
  • The inhibition of necroptosis by poxviruses is critical for viral survival and pathogenesis.
  • This highlights the importance of necroptosis in the host-pathogen evolutionary arms race.