ArticleThe Journal of clinical investigation1998
Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 91 citations in OpenAlex.
- Expression of Toll-like Receptors and Chemokine Receptors in the Early and Advanced Stages of HIV Infection Aggravated byInternational journal of molecular sciences · 2026Article
- S100A14 Is Increased in Activated NK Cells and Plasma of HIV-Exposed Seronegative People Who Inject Drugs and Promotes Monocyte-NK Crosstalk.Journal of acquired immune deficiency syndromes (1999) · 2019Article
- Humoral immune responses to Streptococcus pneumoniae in the setting of HIV-1 infection.Vaccine · 2015Review
- Comparative analysis of the capacity of elite suppressor CD4+ and CD8+ T cells to inhibit HIV-1 replication in monocyte-derived macrophages.Journal of virology · 2014Article
- 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
- Nuclear receptor signaling inhibits HIV-1 replication in macrophages through multiple trans-repression mechanisms.Journal of virology · 2011Article
- Human immunodeficiency virus type-1 group M quasispecies evolution: diversity and divergence in patients co-infected with active tuberculosis.Medical microbiology and immunology · 2010Article
- Neisseria gonorrhoeae enhances HIV-1 infection of primary resting CD4+ T cells through TLR2 activation.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Human peritoneal macrophages from ascitic fluid can be infected by a broad range of HIV-1 isolates.Journal of acquired immune deficiency syndromes (1999) · 2010Article
- Cyclin T1-dependent genes in activated CD4 T and macrophage cell lines appear enriched in HIV-1 co-factors.PloS one · 2008Article
- Bacterial lipopolysaccharide enhances cardiac dysfunction but not retroviral replication in murine AIDS: roles of macrophage infiltration and toll-like receptor 4 expression.The American journal of pathology · 2006Article
- Cell-type-dependent effect of transforming growth factor beta, a major cytokine in breast milk, on human immunodeficiency virus type 1 infection of mammary epithelial MCF-7 cells or macrophages.Journal of virology · 2004Article
- Fcgamma receptor-mediated suppression of human immunodeficiency virus type 1 replication in primary human macrophages.Journal of virology · 2003Article
- Contribution of immune activation to the pathogenesis and transmission of human immunodeficiency virus type 1 infection.Clinical microbiology reviews · 2001Review
- Human immunodeficiency virus type 1 (HIV-1)-induced GRO-alpha production stimulates HIV-1 replication in macrophages and T lymphocytes.Journal of virology · 2001Article
- Cytokine responses to treponema pectinovorum and treponema denticola in human gingival fibroblasts.Infection and immunity · 2000Article
- Cathepsin G, a neutrophil-derived serine protease, increases susceptibility of macrophages to acute human immunodeficiency virus type 1 infection.Journal of virology · 2000Article
- CCR5 signal transduction in macrophages by human immunodeficiency virus and simian immunodeficiency virus envelopes.Journal of virology · 2000Article
- Coreceptor competition for association with CD4 may change the susceptibility of human cells to infection with T-tropic and macrophagetropic isolates of human immunodeficiency virus type 1.Journal of virology · 2000Article
- Mutagenesis of CXCR4 identifies important domains for human immunodeficiency virus type 1 X4 isolate envelope-mediated membrane fusion and virus entry and reveals cryptic coreceptor activity for R5 isolates.Journal of virology · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microbial coinfections variably influence HIV-1 infection through immune activation or direct interaction of microorganisms with HIV-1 or its target cells. In this study, we investigated whether exposure of macrophages to bacterial products impacts the susceptibility of these cells to HIV-1 of different cellular tropisms. We demonstrate that () macrophages exposed to bacterial cell wall components such as lipopolysaccharide (LPS) (Gram-negative rods), lipoteichoic acid (Gram-positive cocci), and lipoarabinomannan (Mycobacteria) become highly susceptible to T cell (T)-tropic HIV-1 (which otherwise poorly replicate in macrophages) and variably susceptible to macrophage (M)-tropic HIV-1; () LPS-stimulated macrophages secrete a number of soluble factors (i.e., chemokines, interferon, and proinflammatory cytokines) that variably affect HIV infection of macrophages, depending on the virus phenotype in question; and () LPS-stimulated macrophages express CCR5 (a major coreceptor for M-tropic HIV-1) at lower levels and CXCR4 (a major coreceptor for T-tropic HIV-1) at higher levels compared with unstimulated macrophages. We hypothesize that a more favorable environment for T-tropic HIV-1 and a less favorable or even unfavorable environment for M-tropic HIV-1 secondary to exposure of macrophages to those bacterial products may accerelate a transition from M- to T-tropic viral phenotype, which is indicative of disease progression.
Indexed as
Identifiers
What OpenQuestion holds
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.