Demystifying Cell Cycle Arrest by HIV-1 Vif

Daniel Salamango, Reuben S. Harris

Research output: Contribution to journalShort surveypeer-review

Abstract

Although APOBEC3 degradation is the canonical function of HIV-1 Vif, this viral protein also induces potent cell cycle arrest through a newly defined mechanism. Here, we review recent advances in this area and propose that the scope of this activity may go beyond subversion of the host cell cycle.

Original languageEnglish (US)
JournalTrends in Microbiology
DOIs
StateAccepted/In press - 2021

Bibliographical note

Funding Information:
This work was supported by National Institute of Allergy and Infectious Diseases (NIAID) R37-AI064046 (to R.S.H.). D.J.S. received salary support from an NIAID K99/R00 transition award (K99-AI147811). R.S.H. is the Margaret Harvey Schering Land Grant Chair for Cancer Research, a Distinguished University McKnight Professor, and an Investigator of the Howard Hughes Medical Institute. R.S.H. is a cofounder, shareholder, and consultant of ApoGen Biotechnologies Inc. D.J.S. has no interests to declare.

Funding Information:
This work was supported by National Institute of Allergy and Infectious Diseases (NIAID) R37-AI064046 (to R.S.H.). D.J.S. received salary support from an NIAID K99/R00 transition award (K99-AI147811). R.S.H. is the Margaret Harvey Schering Land Grant Chair for Cancer Research, a Distinguished University McKnight Professor, and an Investigator of the Howard Hughes Medical Institute .

Keywords

  • G2/M cell cycle arrest
  • HIV-1
  • host–pathogen interaction
  • PPP2R5
  • Vif

PubMed: MeSH publication types

  • Journal Article

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