ArticleJournal of virology2002
Cytopathic killing of peripheral blood CD4(+) T lymphocytes by human immunodeficiency virus type 1 appears necrotic rather than apoptotic and does not require env.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 89 citations in OpenAlex.
- DRAM triggers lysosomal membrane permeabilization and cell death in CD4(+) T cells infected with HIV.PLoS pathogens · 2013Trial
- Elimination of Human Immunodeficiency Virus Reservoirs Harboring Intact Proviruses.The Journal of infectious diseases · 2026Article
- In vitro HIV DNA integration in STAT3 drives T cell persistence-A model of HIV-associated T cell lymphoma.PLoS pathogens · 2025Article
- The HIV-1Viruses · 2024Article
- Extracellular vesicle isolation methods identify distinct HIV-1 particles released from chronically infected T-cells.Journal of extracellular vesicles · 2024Article
- Impact of Chronic HIV Infection on SARS-CoV-2 Infection, COVID-19 Disease and Vaccines.Current HIV/AIDS reports · 2022Review
- Targeting the Latent Reservoir for HIV-1.Immunity · 2018Review
- Casp8p41: The Protean Mediator of Death in CD4 T-cells that Replicate HIV.Journal of cell death · 2016Review
- Broad targeting of resistance to apoptosis in cancer.Seminars in cancer biology · 2015Review
- HIV integrase and the swan song of the CD4 T cells?Retrovirology · 2013Article
- The mechanism of necroptosis in normal and cancer cells.Cancer biology & therapy · 2013Review
- Microbial translocation in the pathogenesis of HIV infection and AIDS.Clinical microbiology reviews · 2013Review
- Prevention of cellular suicide by cytomegaloviruses.Viruses · 2012Review
- Many stimuli pull the necrotic trigger, an overview.Cell death and differentiation · 2012Review
- Exposed hydrophobic residues in human immunodeficiency virus type 1 Vpr helix-1 are important for cell cycle arrest and cell death.PloS one · 2011Article
- Protein kinase A phosphorylation activates Vpr-induced cell cycle arrest during human immunodeficiency virus type 1 infection.Journal of virology · 2010Article
- Model with two types of CTL regulation and experiments on CTL dynamics.Journal of theoretical biology · 2010Article
- Th17 and regulatory T cells: implications for AIDS pathogenesis.Current opinion in HIV and AIDS · 2010Review
- Preferential cytolysis of peripheral memory CD4+ T cells by in vitro X4-tropic human immunodeficiency virus type 1 infection before the completion of reverse transcription.Journal of virology · 2008Article
- Commitment to apoptosis in CD4(+) T lymphocytes productively infected with human immunodeficiency virus type 1 is initiated by lysosomal membrane permeabilization, itself induced by the isolated expression of the viral protein Nef.Journal of virology · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
An important unresolved issue of AIDS pathogenesis is the mechanism of human immunodeficiency virus (HIV)-induced CD4(+) T-lymphocyte destruction. We show here that HIV type 1 (HIV-1) exerts a profound cytopathic effect upon peripheral blood CD4(+) T lymphocytes that resembles necrosis rather than apoptosis. Necrotic cytopathology was found with both laboratory-adapted strains and primary isolates of HIV-1. We carefully investigated the role of env, which has been previously implicated in HIV cytopathicity. HIV-1 stocks with equivalent infectivity were prepared from constructs with either an intact or mutated env coding region and pseudotyped with the glycoprotein of vesicular stomatitis virus (VSV-G) so that the HIV envelope was not rate-limiting for infection. Infected Jurkat T cells died whether or not env was intact; however, the expression of env accelerated death significantly. The accelerated death was blocked by protease inhibitors, indicating that it was due to reinfection by newly produced virus in env(+) cultures. Accordingly, we found no disparity in kinetics in CD4(lo) Jurkat cells. In highly infected peripheral blood T cells, profound necrosis occurred equivalently with both env(+) and env(-) stocks of HIV-1. We also found that HIV-1 cytopathicity was undiminished by the absence of nef. However, viral stocks made by complementation or packaging of HIV-1 genomes with the natural protein-coding sequences replaced by the green fluorescent protein were highly infectious but not cytopathic. Thus, env can accelerate cell death chiefly as an entry function, but one or more viral functions other than env or nef is essential for necrosis of CD4(+) T cells induced by HIV-1.
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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.