ArticleVirology journal2011
Single amino acid change in gp41 region of HIV-1 alters bystander apoptosis and CD4 decline in humanized mice.
Article in Virology journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Combination gene therapy for HIV using a conditional suicidal gene with CCR5 knockout.Virology journal · 2021Article
- The Paradox of HIV Blood-Brain Barrier Penetrance and Antiretroviral Drug Delivery Deficiencies.Trends in neurosciences · 2020Review
- Differential Pathogenicity of SHIV KB9 and 89.6 Env Correlates with Bystander Apoptosis Induction in CD4+ T cells.Viruses · 2019Article
- HIV-1 subtype CRF01_AE and B differ in utilization of low levels of CCR5, Maraviroc susceptibility and potential N-glycosylation sites.Virology · 2017Article
- Review
- 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
- Genetic signatures of HIV-1 envelope-mediated bystander apoptosis.The Journal of biological chemistry · 2014Article
- New generation humanized mice for virus research: comparative aspects and future prospects.Virology · 2013Review
- HIV-1 induced bystander apoptosis.Viruses · 2012Review
- Nef functions in BLT mice to enhance HIV-1 replication and deplete CD4+CD8+ thymocytes.Retrovirology · 2012Article
- The HR2 polymorphism N140I in the HIV-1 gp41 combined with the HR1 V38A mutation is associated with a less cytopathic phenotype.Retrovirology · 2012Article
- Targeting HIV-1 gp41-induced fusion and pathogenesis for anti-viral therapy.Current topics in medicinal chemistry · 2011Review
- HIV ENV glycoprotein-mediated bystander apoptosis depends on expression of the CCR5 co-receptor at the cell surface and ENV fusogenic activity.The Journal of biological chemistry · 2011Article
- The utility of the new generation of humanized mice to study HIV-1 infection: transmission, prevention, pathogenesis, and treatment.Retrovirology · 2011Review
- Humanized mouse models of HIV infection.AIDS reviewsReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe mechanism by which HIV infection leads to a selective depletion of CD4 cells leading to immunodeficiency remains highly debated. Whether the loss of CD4 cells is a direct consequence of virus infection or bystander apoptosis of uninfected cells is also uncertain.
resultsWe have addressed this issue in the humanized mouse model of HIV infection using a HIV variant with a point mutation in the gp41 region of the Env glycoprotein that alters its fusogenic activity. We demonstrate here that a single amino acid change (V38E) altering the cell-to-cell fusion activity of the Env minimizes CD4 loss in humanized mice without altering viral replication. This differential pathogenesis was associated with a lack of bystander apoptosis induction by V38E virus even in the presence of similar levels of infected cells. Interestingly, immune activation was observed with both WT and V38E infection suggesting that the two phenomena are likely not interdependent in the mouse model.
conclusionsWe conclude that Env fusion activity is one of the determinants of HIV pathogenesis and it may be possible to attenuate HIV by targeting gp41.
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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.