ArticlePLoS pathogens2012
Hyperthermia stimulates HIV-1 replication.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 60 citations in OpenAlex.
- Burden of heat stress on residual work capacity among farmers living with chronic HIV in Siaya county, Kenya: a longitudinal observational study protocol.BMC public health · 2025Observational
- Heat shock protein 90 is a chaperone regulator of HIV-1 latency.PLoS pathogens · 2025Article
- Geldanamycin, a Naturally Occurring Inhibitor of Hsp90 and a Lead Compound for Medicinal Chemistry.Journal of medicinal chemistry · 2024Review
- The heat shock response and small molecule regulators.European journal of medicinal chemistry · 2021Review
- Diversity in heat shock protein families: functional implications in virus infection with a comprehensive insight of their role in the HIV-1 life cycle.Cell stress & chaperones · 2021Review
- Effect of a fever in viral infections - the 'Goldilocks' phenomenon?World journal of clinical cases · 2021Review
- Turning up the heat on HIV-1.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- HSF1 Activation Can Restrict HIV Replication.ACS infectious diseases · 2020Article
- Block-And-Lock Strategies to Cure HIV Infection.Viruses · 2020Review
- Proteomic profiling of HIV-1 infection of human CD4Nature microbiology · 2019Article
- Serum deprivation/starvation leads to reactivation of HIV-1 in latently infected monocytes via activating ERK/JNK pathway.Scientific reports · 2018Article
- RIPK1 is a critical modulator of both tonic and TLR-responsive inflammatory and cell death pathways in human macrophage differentiation.Cell death & disease · 2018Article
- Class 1-Selective Histone Deacetylase (HDAC) Inhibitors Enhance HIV Latency Reversal while Preserving the Activity of HDAC Isoforms Necessary for Maximal HIV Gene Expression.Journal of virology · 2018Article
- Quiescence Promotes Latent HIV Infection and Resistance to Reactivation from Latency with Histone Deacetylase Inhibitors.Journal of virology · 2017Article
- Cellular fatty acid synthase is required for late stages of HIV-1 replication.Retrovirology · 2017Article
- The heat shock protein 90 of Toxoplasma gondii is essential for invasion of host cells and tachyzoite growth.Parasite (Paris, France) · 2017Article
- Heat Shock Protein 90 Facilitates Latent HIV Reactivation through Maintaining the Function of Positive Transcriptional Elongation Factor b (p-TEFb) under Proteasome Inhibition.The Journal of biological chemistry · 2016Article
- Article
- Heat Shock Factor 1 Mediates Latent HIV Reactivation.Scientific reports · 2016Article
- Inhibition of Heat Shock Protein 90 Prevents HIV Rebound.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
Abstract
HIV-infected individuals may experience fever episodes. Fever is an elevation of the body temperature accompanied by inflammation. It is usually beneficial for the host through enhancement of immunological defenses. In cultures, transient non-physiological heat shock (42-45°C) and Heat Shock Proteins (HSPs) modulate HIV-1 replication, through poorly defined mechanisms. The effect of physiological hyperthermia (38-40°C) on HIV-1 infection has not been extensively investigated. Here, we show that culturing primary CD4+ T lymphocytes and cell lines at a fever-like temperature (39.5°C) increased the efficiency of HIV-1 replication by 2 to 7 fold. Hyperthermia did not facilitate viral entry nor reverse transcription, but increased Tat transactivation of the LTR viral promoter. Hyperthermia also boosted HIV-1 reactivation in a model of latently-infected cells. By imaging HIV-1 transcription, we further show that Hsp90 co-localized with actively transcribing provirus, and this phenomenon was enhanced at 39.5°C. The Hsp90 inhibitor 17-AAG abrogated the increase of HIV-1 replication in hyperthermic cells. Altogether, our results indicate that fever may directly stimulate HIV-1 replication, in a process involving Hsp90 and facilitation of Tat-mediated LTR activity.
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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.