ArticleJournal of virology1997
Human immunodeficiency virus type 1 Vpr induces apoptosis following cell cycle arrest.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
145 citing papers in PubMed.
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- HIV-1 Vpr Drives a B Cell-Like Phenotype in Primary CD4MedComm · 2026Article
- HIV-1 infection does not confer intrinsic resistance to cell death induced by cytotoxic T lymphocytes.bioRxiv : the preprint server for biology · 2026Article
- HIV-1 accessory protein Vpr possesses a cryptic p300-dependent transcription-promoting activity that is blocked by histone deacetylases in CD4+ T cells.PLoS pathogens · 2025Article
- The HIV-1Viruses · 2024Article
- Vpr driving DNA methylation variation of CD4 + T cells in HIV-1 infection.Virology journal · 2024Article
- HIV-1 Vpr Functions in Primary CD4Viruses · 2024Review
- Vpr attenuates antiviral immune responses and is critical for full pathogenicity of SIViScience · 2023Article
- Tubular-specific expression of HIV protein Vpr leads to severe tubulointerstitial damage accompanied by progressive fibrosis and cystic development.Kidney international · 2023Article
- Article
- The Interplay Among HIV, LINE-1, and the Interferon Signaling System.Frontiers in immunology · 2021Review
- Bioactive Compounds from Medicinal Plants in Myanmar.Progress in the chemistry of organic natural products · 2021Article
- Bovine Leukemia Virus Infection Affects Host Gene Expression Associated with DNA Mismatch Repair.Pathogens (Basel, Switzerland) · 2020Article
- Review
- Article
- Viral protein X reduces the incorporation of mutagenic noncanonical rNTPs during lentivirus reverse transcription in macrophages.The Journal of biological chemistry · 2020Article
- HIV-1 Vif's Capacity To Manipulate the Cell Cycle Is Species Specific.Journal of virology · 2018Article
- Polyploidy and Mitotic Cell Death Are Two Distinct HIV-1 Vpr-Driven Outcomes in Renal Tubule Epithelial Cells.Journal of virology · 2018Article
- Proteasomal Degradation Machinery: Favorite Target of HIV-1 Proteins.Frontiers in microbiology · 2018Review
- Proliferation of latently infected CD4The Journal of experimental medicine · 2017Article
85 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The human immunodeficiency virus type 1 (HIV-1) vpr gene encodes a protein which induces arrest of cells in the G2 phase of the cell cycle. Here, we demonstrate that following the arrest of cells in G2, Vpr induces apoptosis in human fibroblasts, T cells, and primary peripheral blood lymphocytes. Analysis of various mutations in the vpr gene revealed that the extent of Vpr-induced G2 arrest correlated with the levels of apoptosis. However, the alleviation of Vpr-induced G2 arrest by treatment with the drug pentoxifylline did not abrogate apoptosis. Together these studies indicate that induction of G2 arrest, but not necessarily continued arrest in G2, was required for Vpr-induced apoptosis to occur. Finally, Vpr-induced G2 arrest has previously been correlated with inactivation of the Cdc2 kinase. Some models of apoptosis have demonstrated a requirement for active Cdc2 kinase for apoptosis to occur. Here we show that accumulation of the hypophosphorylated or active form of the Cdc2 kinase is not required for Vpr-induced apoptosis. These studies indicate that Vpr is capable of inducing apoptosis, and we propose that both the initial arrest of cells and subsequent apoptosis may contribute to CD4 cell depletion in HIV-1 disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.