ArticlePLoS pathogens2010
Patients with discordant responses to antiretroviral therapy have impaired killing of HIV-infected T cells.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
The trial behind it
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
16 citing papers in PubMed, 21 citations in OpenAlex.
- Long-term SARS-CoV-2 RNA shedding and its temporal association to IgG seropositivity.Cell death discovery · 2020Article
- Long-term SARS-CoV-2 RNA Shedding and its Temporal Association to IgG Seropositivity.medRxiv : the preprint server for health sciences · 2020Article
- Purifying Selection in Human Immunodeficiency Virus-1Journal of clinical medicine research · 2020Article
- HIV Protease-Generated Casp8p41, When Bound and Inactivated by Bcl2, Is Degraded by the Proteasome.Journal of virology · 2018Article
- Prime, Shock, and Kill: Priming CD4 T Cells from HIV Patients with a BCL-2 Antagonist before HIV Reactivation Reduces HIV Reservoir Size.Journal of virology · 2016Article
- Casp8p41: The Protean Mediator of Death in CD4 T-cells that Replicate HIV.Journal of cell death · 2016Review
- Casp8p41 and HIV.Oncotarget · 2015Article
- HIV-1 protease cleaves the serine-threonine kinases RIPK1 and RIPK2.Retrovirology · 2015Article
- Casp8p41 generated by HIV protease kills CD4 T cells through direct Bak activation.The Journal of cell biology · 2014Article
- Review
- Short communication: CD4 T cell declines occurring during suppressive antiretroviral therapy reflect continued production of Casp8p41.AIDS research and human retroviruses · 2014Article
- Choice of antiretroviral therapy differentially impacts survival of HIV-infected CD4 T cells.Molecular and cellular therapies · 2014Article
- Making sense of how HIV kills infected CD4 T cells: implications for HIV cure.Molecular and cellular therapies · 2014Review
- Anti-apoptotic mechanisms of HIV: lessons and novel approaches to curing HIV.Cellular and molecular life sciences : CMLS · 2013Review
- Drug-resistant virus has reduced ability to induce immune activation.Journal of acquired immune deficiency syndromes (1999) · 2012Article
- The HIV-1-specific protein Casp8p41 induces death of infected cells through Bax/Bak.Journal of virology · 2011Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
In medicine, understanding the pathophysiologic basis of exceptional circumstances has led to an enhanced understanding of biology. We have studied the circumstance of HIV-infected patients in whom antiretroviral therapy results in immunologic benefit, despite virologic failure. In such patients, two protease mutations, I54V and V82A, occur more frequently. Expressing HIV protease containing these mutations resulted in less cell death, caspase activation, and nuclear fragmentation than wild type (WT) HIV protease or HIV protease containing other mutations. The impaired induction of cell death was also associated with impaired cleavage of procaspase 8, a requisite event for HIV protease mediated cell death. Primary CD4 T cells expressing I54V or V82A protease underwent less cell death than with WT or other mutant proteases. Human T cells infected with HIV containing these mutations underwent less cell death and less Casp8p41 production than WT or HIV containing other protease mutations, despite similar degrees of viral replication. The reductions in cell death occurred both within infected cells, as well as in uninfected bystander cells. These data indicate that single point mutations within HIV protease which are selected in vivo can significantly impact the ability of HIV to kill CD4 T cells, while not impacting viral replication. Therefore, HIV protease regulates both HIV replication as well as HIV induced T cell depletion, the hallmark of HIV pathogenesis.
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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.