Journal
VIRUSES-BASEL
Volume 13, Issue 8, Pages -Publisher
MDPI
DOI: 10.3390/v13081466
Keywords
human immunodeficiency virus-1 and-2; simian immunodeficiency viruses; viral protein U (Vpu); bone marrow stromal antigen 2; transmembrane domain; endoplasmic reticulum-associated degradation pathway; endosomal sorting complexes required for transport; endolysosomes; autophagy
Categories
Funding
- National Institute of Health (NIH), USA [P30GM100329, U54GM115458, R01MH100972, R01MH105329, R01MH119000, 2R01NS065957, 2R01DA032444]
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HIV-1 and HIV-2 originated from cross-species transmission of simian immunodeficiency viruses (SIVs), with one transmission event involving SIVcpz from chimpanzees giving rise to group M HIV-1 responsible for the AIDS pandemic. Vpu is an HIV-1 accessory protein localized in cells capable of being infected by HIV-1 and regulates infection and transmission by downregulating BST-2, CD4 proteins levels, and immune evasion.
Human immunodeficiency virus (HIV)-1 and HIV-2 originated from cross-species transmission of simian immunodeficiency viruses (SIVs). Most of these transfers resulted in limited spread of these viruses to humans. However, one transmission event involving SIVcpz from chimpanzees gave rise to group M HIV-1, with M being the principal strain of HIV-1 responsible for the AIDS pandemic. Vpu is an HIV-1 accessory protein generated from Env/Vpu encoded bicistronic mRNA and localized in cytosolic and membrane regions of cells capable of being infected by HIV-1 and that regulate HIV-1 infection and transmission by downregulating BST-2, CD4 proteins levels, and immune evasion. This review will focus of critical aspects of Vpu including its zoonosis, the adaptive hurdles to cross-species transmission, and future perspectives and broad implications of Vpu in HIV-1 infection and dissemination.
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