ArticleJournal of virology2002
A soluble factor(s) secreted from CD8(+) T lymphocytes inhibits human immunodeficiency virus type 1 replication through STAT1 activation.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 60 citations in OpenAlex.
- The STAT Signaling Pathway in HIV-1 Infection: Roles and Dysregulation.International journal of molecular sciences · 2025Review
- Attenuated Dengue virus PV001-DV induces oncolytic tumor cell death and potent immune responses.Journal of translational medicine · 2023Article
- Role of CXCR5Frontiers in microbiology · 2022Review
- Non-cytotoxic functions of CD8 T cells: "repentance of a serial killer".Frontiers in immunology · 2022Review
- The CD8Microbiology and molecular biology reviews : MMBR · 2021Review
- Cathepsins and Their Endogenous Inhibitors in Host Defense DuringFrontiers in immunology · 2021Review
- Canonical Wnts Mediate CD8Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Mechanisms of CD8European journal of immunology · 2018Review
- Article
- Macrophage derived cystatin B/cathepsin B in HIV replication and neuropathogenesis.Current HIV research · 2014Review
- CD8(+) lymphocytes suppress human immunodeficiency virus 1 replication by secreting type I interferons.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2013Article
- CD8(+) T-cell effector function and transcriptional regulation during HIV pathogenesis.Immunological reviews · 2013Review
- Inhibition of interferon response by cystatin B: implication in HIV replication of macrophage reservoirs.Journal of neurovirology · 2012Article
- Proteomic analysis of HIV-infected macrophages.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Review
- Secretion of MIP-1β and MIP-1α by CD8(+) T-lymphocytes correlates with HIV-1 inhibition independent of coreceptor usage.Cellular immunology · 2011Article
- Adenovirus vectors block human immunodeficiency virus-1 replication in human alveolar macrophages by inhibition of the long terminal repeat.American journal of respiratory cell and molecular biology · 2010Article
- Cystatin B associates with signal transducer and activator of transcription 1 in monocyte-derived and placental macrophages.Placenta · 2009Article
- Noncytotoxic suppression of human immunodeficiency virus type 1 transcription by exosomes secreted from CD8+ T cells.Journal of virology · 2009Article
- SOCS1 is an inducible host factor during HIV-1 infection and regulates the intracellular trafficking and stability of HIV-1 Gag.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- SAMMA, a mandelic acid condensation polymer, inhibits dendritic cell-mediated HIV transmission.FEBS letters · 2007Article
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 at 2 institutions in 1 country.
Funding
Abstract
CD8(+) T lymphocytes can suppress human immunodeficiency virus type 1 (HIV-1) replication by secreting a soluble factor(s) known as CD8(+) T-lymphocyte antiviral factor (CAF). One site of CAF action is inhibition of HIV-1 RNA transcription, particularly at the step of long terminal repeat (LTR)-driven gene expression. However, the mechanism by which CAF inhibits LTR activation is not understood. Here, we show that conditioned media from several herpesvirus saimari-transformed CD8(+) T lymphocytes inhibit, in a time- and dose-dependent manner, the replication of HIV-1 pseudotype viruses that express the envelope glycoproteins of vesicular stomatitis virus (HIV-1(VSV)). The same conditioned media also inhibit phorbol myristate acetate-induced activation of the HIV-1 LTR and activate the signal transducer and activator of transcription 1 (STAT1) protein. We have obtained direct evidence that STAT1 is necessary for CAF-mediated inhibition of LTR activation and HIV-1 replication. Thus, the inhibitory effect of CAF on HIV-1(VSV) replication was abolished in STAT1-deficient cells. Moreover, CAF inhibition of LTR activation was diminished both in STAT1-deficient cells and in cells expressing a STAT1 dominant negative mutant but was restored when STAT1 was reintroduced into the STAT1-deficient cells. We also observed that CAF induced the expression of interferon regulatory factor 1 (IRF-1), and that IRF-1 gene induction was STAT-1 dependent. Taken together, our results suggest that CAF activates STAT1, leading to IRF-1 induction and inhibition of gene expression regulated by the HIV-1 LTR. This study therefore helps clarify one molecular mechanism of host defense against HIV-1.
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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.