ArticleThe Journal of biological chemistry2011
HIV ENV glycoprotein-mediated bystander apoptosis depends on expression of the CCR5 co-receptor at the cell surface and ENV fusogenic activity.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Combination gene therapy for HIV using a conditional suicidal gene with CCR5 knockout.Virology journal · 2021Article
- Differential Pathogenicity of SHIV KB9 and 89.6 Env Correlates with Bystander Apoptosis Induction in CD4+ T cells.Viruses · 2019Article
- MiR-455-5p Suppresses the Progression of Prostate Cancer by Targeting CCR5.BioMed research international · 2019Article
- Low level expression of the Mitochondrial Antiviral Signaling protein (MAVS) associated with long-term nonprogression in SIV-infected rhesus macaques.Virology journal · 2018Article
- HIV-1 subtype CRF01_AE and B differ in utilization of low levels of CCR5, Maraviroc susceptibility and potential N-glycosylation sites.Virology · 2017Article
- Development of Virus-Like-Particle Vaccine and Reporter Assay for Zika Virus.Journal of virology · 2017Article
- HIV-infected macrophages and microglia that survive acute infection become viral reservoirs by a mechanism involving Bim.Scientific reports · 2017Article
- Review
- CCR5 promoter activity correlates with HIV disease progression by regulating CCR5 cell surface expression and CD4 T cell apoptosis.Scientific reports · 2017Article
- Class B β-arrestin2-dependent CCR5 signalosome retention with natural antibodies to CCR5.Scientific reports · 2016Article
- CCR5 interaction with HIV-1 Env contributes to Env-induced depletion of CD4 T cells in vitro and in vivo.Retrovirology · 2016Article
- HIV-1 Env Glycoprotein Phenotype along with Immune Activation Determines CD4 T Cell Loss in HIV Patients.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Review
- A quantitative comparison of anti-HIV gene therapy delivered to hematopoietic stem cells versus CD4+ T cells.PLoS computational biology · 2014Article
- Induction of HIV-blocking anti-CCR5 IgA in Peyers's patches without histopathological alterations.Journal of virology · 2014Article
- The majority of CD4+ T-cell depletion during acute simian-human immunodeficiency virus SHIV89.6P infection occurs in uninfected cells.Journal of virology · 2014Article
- Genetic signatures of HIV-1 envelope-mediated bystander apoptosis.The Journal of biological chemistry · 2014Article
- HIV-1 induced bystander apoptosis.Viruses · 2012Review
- Macroautophagy Regulation during HIV-1 Infection of CD4+ T Cells and Macrophages.Frontiers in immunology · 2012Article
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-1 infections lead to a progressive depletion of CD4 cells culminating in AIDS. The coreceptor usage by HIV varies from CCR5 (R5) tropic early in infection to CXCR4 (X4) tropic in later infections. Although the coreceptor switch from R5 to X4 tropic HIV is well associated with progression to AIDS, the role of CCR5 in disease progression especially in patients infected exclusively with R5 isolates throughout the disease remains enigmatic. To better understand the role of CCR5 and R5 tropic HIV envelope in AIDS pathogenesis, we asked whether the levels of CCR5 and/or HIV Env-mediated fusion determine apoptosis of bystander cells. We generated CD4(+) T cell lines expressing varying levels of CCR5 on the cell surface to show that CCR5 expression levels correlate with bystander apoptosis induction. The mechanism of apoptosis involved caspase-3 activation and mitochondrial depolarization and was dependent on gp41 fusion activity as confirmed by fusion-restricted gp41 point mutants and use of the fusion inhibitor T20. Interestingly, lower levels of CCR5 were able to support virus replication in the absence of bystander apoptosis. Our findings suggest that R5 HIV-1-mediated bystander apoptosis is dependent on both CCR5 expression levels as well as fusogenic activity of the Env glycoprotein.
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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.