ArticleJournal of virology1998
Endogenous production of beta-chemokines by CD4+, but not CD8+, T-cell clones correlates with the clinical state of human immunodeficiency virus type 1 (HIV-1)-infected individuals and may be responsible for blocking infection with non-syncytium-inducing HIV-1 in vitro.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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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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
37 citing papers in PubMed, 118 citations in OpenAlex.
- Host Genetic Impact on Infectious Diseases among Different Ethnic Groups.Advanced genetics (Hoboken, N.J.) · 2023Review
- Omic Technologies in HIV: Searching Transcriptional Signatures Involved in Long-Term Non-Progressor and HIV Controller Phenotypes.Frontiers in immunology · 2022Review
- Transcriptional down-regulation ofeLife · 2019Article
- Mechanisms of Virologic Control and Clinical Characteristics of HIV+ Elite/Viremic Controllers.The Yale journal of biology and medicine · 2017Review
- RANTES Gene Polymorphisms Associated with HIV-1 Infections in Kenyan Population.Disease markers · 2016Article
- Increased Levels of Macrophage Inflammatory Proteins Result in Resistance to R5-Tropic HIV-1 in a Subset of Elite Controllers.Journal of virology · 2015Article
- Host Factors and HIV-1 Replication: Clinical Evidence and Potential Therapeutic Approaches.Frontiers in immunology · 2013Review
- CD8(+) T-cell effector function and transcriptional regulation during HIV pathogenesis.Immunological reviews · 2013Review
- Natural Scrub Typhus Antibody Suppresses HIV CXCR4(X4) Viruses.Infectious disease reports · 2013Review
- Can non-lytic CD8+ T cells drive HIV-1 escape?PLoS pathogens · 2013Article
- Cell-Mediated Immunity in Elite Controllers Naturally Controlling HIV Viral Load.Frontiers in immunology · 2013Article
- Secretion of MIP-1β and MIP-1α by CD8(+) T-lymphocytes correlates with HIV-1 inhibition independent of coreceptor usage.Cellular immunology · 2011Article
- M-tropic HIV envelope protein gp120 exhibits a different neuropathological profile than T-tropic gp120 in rat striatum.The European journal of neuroscience · 2010Article
- Polymorphisms in toll-like receptor 4 and toll-like receptor 9 influence viral load in a seroincident cohort of HIV-1-infected individuals.AIDS (London, England) · 2009Article
- Host genetics influences on HIV type-1 disease.Antiviral therapy · 2009Review
- Antigen stimulation induces HIV envelope gp120-specific CD4(+) T cells to secrete CCR5 ligands and suppress HIV infection.Virology · 2007Article
- Longitudinal comparison of chemokines in breastmilk early postpartum among HIV-1-infected and uninfected Kenyan women.Breastfeeding medicine : the official journal of the Academy of Breastfeeding Medicine · 2007Article
- Host factors influencing susceptibility to HIV infection and AIDS progression.Retrovirology · 2007Review
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Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Recent studies have demonstrated that the beta-chemokines RANTES, MIP-1alpha, and MIP-1beta suppress human immunodeficiency virus type 1 (HIV-1) replication in vitro and may play an important role in protecting exposed but uninfected individuals from HIV-1 infection. However, levels of beta-chemokines in AIDS patients are comparable to and can exceed levels in nonprogressing individuals, indicating that global beta-chemokine production may have little effect on HIV-1 disease progression. We sought to clarify the role of beta-chemokines in nonprogressors and AIDS patients by examination of beta-chemokine production and HIV-1 infection in patient T-lymphocyte clones established by herpesvirus saimiri immortalization. Both CD4+ and CD8+ clones were established, and they resembled primary T cells in their phenotypes and expression of activated T-cell markers. CD4+ T-cell clones from all patients had normal levels of mRNA-encoding CCR5, a coreceptor for non-syncytium-inducing (NSI) HIV-1. CD4+ clones from nonprogressors and CD8+ clones from AIDS patients secreted high levels of RANTES, MIP1alpha, and MIP-1beta. In contrast, CD4+ clones from AIDS patients produced no RANTES and little or no MIP-1alpha or MIP-1beta. The infection of CD4+ clones with the NSI HIV-1 strain ADA revealed an inverse correlation to beta-chemokine production; clones from nonprogressors were poorly susceptible to ADA replication, but clones from AIDS patients were highly infectable. The resistance to ADA infection in CD4+ clones from nonprogressors could be partially reversed by treatment with anti-beta-chemokine antibodies. These results indicate that CD4+ cells can be protected against NSI-HIV-1 infection in culture through endogenously produced factors, including beta-chemokines, and that beta-chemokine production by CD4+, but not CD8+, T cells may constitute one mechanism of disease-free survival for HIV-1-infected individuals.
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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.