ArticlePloS one2008
Infected cell killing by HIV-1 protease promotes NF-kappaB dependent HIV-1 replication.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 25 citations in OpenAlex.
- Scopoletin Reactivates Latent HIV-1 by Inducing NF-κB Expression without Global T Cell Activation.International journal of molecular sciences · 2023Article
- PEBP1 suppresses HIV transcription and induces latency by inactivating MAPK/NF-κB signaling.EMBO reports · 2020Article
- Mechanisms of Human Immunodeficiency Virus-Associated Lymphocyte Regulated Cell Death.AIDS research and human retroviruses · 2020Review
- TRAILshort Protects against CD4 T Cell Death during Acute HIV Infection.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Maintenance of the HIV Reservoir Is Antagonized by Selective BCL2 Inhibition.Journal of virology · 2017Article
- 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
- Article
- Leveraging Cancer Therapeutics for the HIV Cure Agenda: Current Status and Future Directions.Drugs · 2015Review
- Renin modulates HIV replication in T cells.Journal of leukocyte 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
- Making sense of how HIV kills infected CD4 T cells: implications for HIV cure.Molecular and cellular therapies · 2014Review
- Choice of antiretroviral therapy differentially impacts survival of HIV-infected CD4 T cells.Molecular and cellular therapies · 2014Article
- Anti-apoptotic mechanisms of HIV: lessons and novel approaches to curing HIV.Cellular and molecular life sciences : CMLS · 2013Review
- Altering cell death pathways as an approach to cure HIV infection.Cell death & disease · 2013Review
- Article
- Isolation of a TRAIL antagonist from the serum of HIV-infected patients.The Journal of biological chemistry · 2011Article
- The HIV-1-specific protein Casp8p41 induces death of infected cells through Bax/Bak.Journal of virology · 2011Article
- Intracellular Casp8p41 content is inversely associated with CD4 T cell count.The Journal of infectious diseases · 2010Article
- Casp8p41 expression in primary T cells induces a proinflammatory response.AIDS (London, England) · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Acute HIV-1 infection of CD4 T cells often results in apoptotic death of infected cells, yet it is unclear what evolutionary advantage this offers to HIV-1. Given the independent observations that acute T cell HIV-1 infection results in (1) NF-kappaB activation, (2) caspase 8 dependent apoptosis, and that (3) caspase 8 directly activates NF-kappaB, we questioned whether these three events might be interrelated. We first show that HIV-1 infected T cell apoptosis, NF-kappaB activation, and caspase 8 cleavage by HIV-1 protease are coincident. Next we show that HIV-1 protease not only cleaves procaspase 8, producing Casp8p41, but also independently stimulates NF-kappaB activity. Finally, we demonstrate that the HIV protease cleavage of caspase 8 is necessary for optimal NF-kappaB activation and that the HIV-1 protease specific cleavage fragment Casp8p41 is sufficient to stimulate HIV-1 replication through NF-kappaB dependent HIV-LTR activation both in vitro as well as in cells from HIV infected donors. Consequently, the molecular events which promote death of HIV-1 infected T cells function dually to promote HIV-1 replication, thereby favoring the propagation and survival of HIV-1.
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What OpenQuestion holds
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.