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 language | English (US) |
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Pages (from-to) | 381-384 |
Number of pages | 4 |
Journal | Trends in Microbiology |
Volume | 29 |
Issue number | 5 |
DOIs | |
State | Published - May 1 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 .
Publisher Copyright:
© 2021 Elsevier Ltd
Keywords
- G2/M cell cycle arrest
- HIV-1
- PPP2R5
- Vif
- host–pathogen interaction