ArticleJournal of molecular medicine (Berlin, Germany)1995
Inhibition of HIV-1 expression by HIV-2.
Article in Journal of molecular medicine (Berlin, Germany), 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Co-Infections and Superinfections between HIV-1 and Other Human Viruses at the Cellular Level.Pathogens (Basel, Switzerland) · 2024Review
- HIV-2 inhibits HIV-1 gene expression via two independent mechanisms during cellular co-infection.Journal of virology · 2023Article
- Insight into HIV-2 latency may disclose strategies for a cure for HIV-1 infection.Journal of virus eradication · 2017Article
- HIV-1 outcompetes HIV-2 in dually infected Senegalese individuals with low CD4⁺ cell counts.AIDS (London, England) · 2013Article
- In vitro correlates of HIV-2-mediated HIV-1 protection.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Potent inhibition of human immunodeficiency virus type 1 (HIV-1) gene expression and virus production by an HIV-2 tat activation-response RNA decoy.Journal of virology · 1999Article
- The sequence and structure of the 3' arm of the first stem-loop of the human immunodeficiency virus type 2 trans-activation responsive region mediate Tat-2 transactivation.Journal of virology · 1997Article
- A potentially novel approach for the gene therapy of HIV-1 disease.Journal of molecular medicine (Berlin, Germany) · 1995Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-1 and HIV-2 are co-endemic in certain geographic areas. HIV-2 is more weakly pathogenic than HIV-1, and progression to AIDS occurs less frequently and over a longer period of time. Recent epidemiologic studies suggest that individuals infected with HIV-2 have a lower risk of HIV-1 infection. Both immune mechanisms and various modes of viral interference have been proposed to account for these results. Our findings, described in this paper, suggest that HIV-2 inhibits HIV-1 replication. To study the molecular interactions between HIV-1 and HIV-2, proviral clones were transfected alone or in combination into the human T cell line CEM. LTR-CAT indicator constructs were included for the purpose of monitoring viral promoter activity. Viral replication in transfected cells was monitored by p24 antigen capture assay of cell culture supernatants and Western blot analysis of cell extracts. HIV-2 inhibited HIV-1 replication as determined by intracellular and extracellular p24 antigen levels. Similar results were obtained with simultaneous virus infection using HIV-1 and HIV-2, rather than transfections of proviral DNA. Using cotransfection of HIV-1 and HIV-2 LTR indicator gene constructs, the mechanism of inhibition was found to be suppression of the HIV-1 LTR by HIV-2. The inhibitory effect of HIV-2 is not due to Tat-2, but appears to discriminate between the HIV-1 and HIV-2 LTRs based on differences in the Tat activation response element, TAR. These results suggest both a molecular mechanism for HIV-2 interference with HIV-1 replication and a potential molecular approach to therapy.
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Registered trials
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