ArticleJournal of virology2007
Vpr cytopathicity independent of G2/M cell cycle arrest in human immunodeficiency virus type 1-infected CD4+ T cells.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
- Article
- Article
- The HIV-1Viruses · 2024Article
- HIV-1 Vpr Functions in Primary CD4Viruses · 2024Review
- Review
- Huntingtin-Interacting Protein 1 Promotes Vpr-Induced G2 Arrest and HIV-1 Infection in Macrophages.Viruses · 2021Article
- HIV-1 Gag Recruits Oligomeric Vpr via Two Binding Sites in p6, but Both Mature p6 and Vpr Are Rapidly Lost upon Target Cell Entry.Journal of virology · 2021Article
- Reprogramming Extracellular Vesicles for Protein Therapeutics Delivery.Pharmaceutics · 2021Article
- A distinct class of plant and animal viral proteins that disrupt mitosis by directly interrupting the mitotic entry switch Wee1-Cdc25-Cdk1.Science advances · 2020Article
- Promiscuous Targeting of Cellular Proteins by Vpr Drives Systems-Level Proteomic Remodeling in HIV-1 Infection.Cell reports · 2019Article
- The HIV-1 Vpr Protein: A Multifaceted Target for Therapeutic Intervention.International journal of molecular sciences · 2017Review
- Defining the roles for Vpr in HIV-1-associated neuropathogenesis.Journal of neurovirology · 2016Review
- Virion encapsidated HIV-1 Vpr induces NFAT to prime non-activated T cells for productive infection.Open biology · 2016Article
- HIV-1 Vpr-a still "enigmatic multitasker".Frontiers in microbiology · 2014Review
- HIV-1 causes CD4 cell death through DNA-dependent protein kinase during viral integration.Nature · 2013Article
- Article
- Evidence for Vpr-dependent HIV-1 replication in human CD4+ CEM.NKR T-cells.Retrovirology · 2012Article
- Article
- Cellular phenotype impacts human immunodeficiency virus type 1 viral protein R subcellular localization.Virology journal · 2011Article
- Molecular insight into how HIV-1 Vpr protein impairs cell growth through two genetically distinct pathways.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanism of CD4(+) T-cell depletion in human immunodeficiency virus type 1 (HIV-1)-infected individuals remains unknown, although mounting evidence suggests that direct viral cytopathicity contributes to this loss. The HIV-1 Vpr accessory protein causes cell death and arrests cells in the G(2)/M phase; however, the molecular mechanism underlying these properties is not clear. Mutation of hydrophobic residues on the surface of its third alpha-helix disrupted Vpr toxicity, G(2)/M arrest induction, nuclear localization, and self-association, implicating this region in multiple Vpr functions. Cytopathicity by virion-delivered mutant Vpr protein correlated with G(2)/M arrest induction but not nuclear localization or self-association. However, infection with whole virus encoding these Vpr mutants did not abrogate HIV-1-induced cell killing. Rather, mutant Vpr proteins that are impaired for G(2)/M block still prevented infected cell proliferation, and this property correlated with the death of infected cells. Chemical agents that inhibit infected cells from entering G(2)/M also did not reduce HIV-1 cytopathicity. Combined, these data implicate Vpr in HIV-1 killing through a mechanism involving inhibiting cell division but not necessarily in G(2)/M. Thus, the hydrophobic region of the third alpha-helix of Vpr is crucial for mediating G(2)/M arrest, nuclear localization, and self-association but dispensable for HIV-1 cytopathicity due to residual cell proliferation blockade mediated by a separate region of the protein.
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