Journal
EXPERIMENTAL BIOLOGY AND MEDICINE
Volume 242, Issue 8, Pages 850-858Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1535370217697384
Keywords
Viral protein U; human immunodeficiency virus type 1; acquired immunodeficiency syndrome; simian immunodeficiency virus; virus; accessory protein
Categories
Funding
- CREST, JST
- Takeda Science Foundation
- Uehara Memorial Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- JSPS [15K07166, 16KT0111]
- MEXT [24115008]
- AMED [16fk0410203h002]
- Grants-in-Aid for Scientific Research [24115008, 16KT0111, 15K07166, 17H05813] Funding Source: KAKEN
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Human immunodeficiency virus type 1 (HIV-1), the causative agent of acquired immunodeficiency syndrome, encodes four accessory genes, one of which is viral protein U (Vpu). Recently, the study of Vpu has been of great interest. For instance, various cellular proteins are degraded (e.g. CD4) and down-modulated (e.g. tetherin) by Vpu. Vpu also antagonizes the function of tetherin and inhibits NF-kappa B. Moreover, Vpu is a viroporin forming ion channels and may represent a promising target for anti-HIV-1 drugs. In this review, we summarize the domains/residues that are responsible for Vpu's functions, describe the current understanding of the role of Vpu in HIV-1-infected cells, and review the effect of Vpu on HIV-1 in replication and pathogenesis. Future investigations that simultaneously assess a combination of Vpu functions are required to clearly delineate the most important functions for viral replication.
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