ArticleProceedings of the National Academy of Sciences of the United States of America1998
Mycobacterium avium complex augments macrophage HIV-1 production and increases CCR5 expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 87 citations in OpenAlex.
- A New Type of Nonsuppressible Viremia Produced by HIV-Infected Macrophage.The Journal of infectious diseases · 2026Article
- A New Type of Nonsuppressible Viremia Produced by HIV-Infected Macrophage.bioRxiv : the preprint server for biology · 2025Article
- Protein ArginineViruses · 2020Article
- Early Epstein-Barr Virus Genomic Diversity and Convergence toward the B95.8 Genome in Primary Infection.Journal of virology · 2018Article
- High glucose enhances HIV entry into T cells through upregulation of CXCR4.Journal of leukocyte biology · 2013Article
- Revising the Role of Myeloid cells in HIV Pathogenesis.Current HIV/AIDS reports · 2013Article
- Modulation of innate host factors by Mycobacterium avium complex in human macrophages includes interleukin 17.The Journal of infectious diseases · 2012Article
- Proline-proline-glutamic acid (PPE) protein Rv1168c of Mycobacterium tuberculosis augments transcription from HIV-1 long terminal repeat promoter.The Journal of biological chemistry · 2012Article
- Leishmania induces survival, proliferation and elevated cellular dNTP levels in human monocytes promoting acceleration of HIV co-infection.PLoS pathogens · 2012Article
- Stromal down-regulation of macrophage CD4/CCR5 expression and NF-κB activation mediates HIV-1 non-permissiveness in intestinal macrophages.PLoS pathogens · 2011Article
- HIV infection and specific mucosal immunity: workshop 4B.Advances in dental research · 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
- Human immunodeficiency virus-1 evolutionary patterns associated with pathogenic processes in the brain.Journal of neurovirology · 2010Article
- Macrophages in vaginal but not intestinal mucosa are monocyte-like and permissive to human immunodeficiency virus type 1 infection.Journal of virology · 2009Article
- Cellular reservoirs of HIV-1 and their role in viral persistence.Current HIV research · 2008Review
- The effects of early syphilis on CD4 counts and HIV-1 RNA viral loads in blood and semen.Sexually transmitted infections · 2005Article
- Human immunodeficiency virus type 1-induced macrophage gene expression includes the p21 gene, a target for viral regulation.Journal of virology · 2005Article
- Secretory leukocyte protease inhibitor binds to annexin II, a cofactor for macrophage HIV-1 infection.The Journal of experimental medicine · 2004Article
- In vitro comparison of topical microbicides for prevention of human immunodeficiency virus type 1 transmission.Antimicrobial agents and chemotherapy · 2004Article
- Contribution of immune activation to the pathogenesis and transmission of human immunodeficiency virus type 1 infection.Clinical microbiology reviews · 2001Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Infection with HIV-1 results in pronounced immune suppression and susceptibility to opportunistic infections (OI). Reciprocally, OI augment HIV-1 replication. As we have shown for Mycobacterium avium complex (MAC) and Pneumocystis carinii, macrophages infected with opportunistic pathogens and within lymphoid tissues containing OI, exhibit striking levels of viral replication. To explore potential underlying mechanisms for increased HIV-1 replication associated with coinfection, blood monocytes were exposed to MAC antigens (MAg) or viable MAC and their levels of tumor necrosis factor alpha (TNFalpha) and HIV-1 coreceptors monitored. MAC enhanced TNFalpha production in vitro, consistent with its expression in coinfected lymph nodes. Using a polyclonal antibody to the CCR5 coreceptor that mediates viral entry of macrophage tropic HIV-1, a subset of unstimulated monocytes was shown to be CCR5-positive by fluorescence-activated cell sorter analysis. After stimulation with MAg or infection with MAC, CCR5 expression was increased at both the mRNA level and on the cell surface. Up-regulation of CCR5 by MAC was not paralleled by an increase in the T cell tropic coreceptor, CXCR4. Increases in NF-kappaB, TNFalpha, and CCR5 were consistent with the enhanced production of HIV-1 in MAg-treated adherent macrophage cultures as measured by HIV-1 p24 levels. Increased CCR5 was also detected in coinfected lymph nodes as compared with tissues with only HIV-1. The increased production of TNFalpha, together with elevated expression of CCR5, provide potential mechanisms for enhanced infection and replication of HIV-1 by macrophages in OI-infected cells and tissues. Consequently, treating OI may inhibit not only the OI-induced pathology, but also limit the viral burden.
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