ArticleJournal of virology2009
Human regulatory T cells are targets for human immunodeficiency Virus (HIV) infection, and their susceptibility differs depending on the HIV type 1 strain.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.
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
68 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Effects of Schistosoma haematobium infection and treatment on the systemic and mucosal immune phenotype, gene expression and microbiome: A systematic review.PLoS neglected tropical diseases · 2024Pooled it
- Effects of schistosomes on host anti-viral immune response and the acquisition, virulence, and prevention of viral infections: A systematic review.PLoS pathogens · 2021Pooled it
- Forkhead box protein 3(+) regulatory T cells and Helios(+) subset in perinatally acquired HIV.Clinical and experimental immunology · 2015Trial
- CCR5 antagonism impacts vaccination response and immune profile in HIV-1 infection.Molecular medicine (Cambridge, Mass.) · 2012Trial
- Trial
- Variation in antiviral immunity and inflammation pathways precedes HIV-1 infection in a high-risk African cohort.The Journal of clinical investigation · 2026Article
- Review
- Regulatory T cells modulate monocyte functions in immunocompetent antiretroviral therapy naive HIV-1 infected people.BMC immunology · 2024Article
- Evolving mechanisms and presentations of cardiovascular disease in people with HIV: implications for management.Clinical microbiology reviews · 2024Review
- Cenicriviroc prevents dysregulation of astrocyte/endothelial cross talk induced by ischemia and HIV-1 via inhibiting the NLRP3 inflammasome and pyroptosis.American journal of physiology. Cell physiology · 2024Article
- Impact ofFrontiers in microbiology · 2023Article
- Preterm Birth in Women With HIV: The Role of the Placenta.Frontiers in global women's health · 2022Review
- Review
- Nanotechnology-based approaches for emerging and re-emerging viruses: Special emphasis on COVID-19.Microbial pathogenesis · 2021Review
- Deciphering DNA Methylation in HIV Infection.Frontiers in immunology · 2021Review
- HIV-Related Immune Activation and Inflammation: Current Understanding and Strategies.Journal of immunology research · 2021 · on this mapReview
- Nonhuman Primate Testing of the Impact of Different Regulatory T Cell Depletion Strategies on Reactivation and Clearance of Latent Simian Immunodeficiency Virus.Journal of virology · 2020Article
- Harnessing regulatory T cell neuroprotective activities for treatment of neurodegenerative disorders.Molecular neurodegeneration · 2020Review
- Single-Cell Technologies Applied to HIV-1 Research: Reaching Maturity.Frontiers in microbiology · 2020Review
- Schistosoma mansoni soluble egg antigen (SEA) and recombinant Omega-1 modulate induced CD4+ T-lymphocyte responses and HIV-1 infection in vitro.PLoS pathogens · 2019Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Regulatory T cells (Treg) are a subpopulation of CD4(+) T cells characterized by the suppressive activity they exert on effector immune responses, including human immunodeficiency virus (HIV)-specific immune responses. Because Treg express CXCR4 and CCR5, they represent potential targets for HIV; however, Treg susceptibility to HIV infection is still unclear. We therefore performed an extensive study of Treg susceptibility to HIV, using lab strains and primary isolates with either CCR5 or CXCR4 tropism. Furthermore, we quantified HIV infection at early and late time points of the virus life cycle. We found that Treg were clearly susceptible to HIV infection. Circulating Treg were not preferentially infected with HIV compared to effector T cells (Teff) in vivo. Conversely, in vitro infection with either CCR5-using (R5) or CXCR4-using (X4) viruses occurred with different dynamics. For instance, HIV infection by R5 viruses (lab strains and primary isolates) resulted in lower levels of infection in Treg compared with Teff at both early and late time points. In contrast, X4 viruses induced higher levels of infection in Treg compared to Teff at early time points, but this difference disappeared at the late time points of the virus life cycle. Our results suggest that the relative susceptibility of Treg to HIV infection compared to Teff varies, depending on both viral and host factors. These variations may play an important role in 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.