Mycobacterium tuberculosis-induced CXCR4 and chemokine expression leads to preferential X4 HIV-1 replication in human macrophages

Hoshino, Yuki; Tse, David K.; Rochford, Gemma; Prabhakar, Savita; Hoshino, Satomi; Chitkara, N. L.; Kuwabara, Kenichi; Ching, Elbert; Raju, Bindu; Gold, Jeffrey A.; Borkowsky, W; Rom, WN; Pine, Richard; Weiden, Michael D.

doi:10.4049/jimmunol.177.12.8874

Cited by 15 publications

(27 citation statements)

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“…After a final wash, the samples were mounted with VectraShield mounting medium (Vector Laboratories), and images were obtained and quantified by Leica TCS NT imaging software for a Leica DM RBE confocal microscope. All data were collected by sequential image recording mode, to prevent 2-photon combination [21].…”

Section: Study Populationmentioning

confidence: 99%

“…They were washed 3 times with PBS and were incubated with and without M. tuberculosis TN913 (a clinical isolate obtained from the PHRI Tuberculosis Center) at an MOI of 3, with and without fresh PMNs (PMN:THP-1, 3:1) and with and without an insert. After 3 days' incubation, HIV-1 RNA was extracted from the supernatants and was assayed as an HIV-1 load by measurement of HIV-1 complementary DNA by use of real-time quantitative polymerase chain reaction assay performed using ABI Prism 7770, as described elsewhere [20,21].…”

Section: Study Populationmentioning

confidence: 99%

See 1 more Smart Citation

Mechanisms of Polymorphonuclear Neutrophil–Mediated Induction of HIV‐1 Replication in Macrophages during Pulmonary Tuberculosis

Hoshino

Gold

et al. 2007

J INFECT DIS

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Section: Study Populationmentioning

confidence: 99%

Section: Study Populationmentioning

confidence: 99%

Mechanisms of Polymorphonuclear Neutrophil–Mediated Induction of HIV‐1 Replication in Macrophages during Pulmonary Tuberculosis

Hoshino

Gold

et al. 2007

J INFECT DIS

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“…In one in vitro study [47], it was observed that MTB increased CXCR4 surface expression on alveolar macrophages and allowed the entry and replication of X4 viruses while inhibiting R5 virus entry. Some earlier studies indicated that macrophages exposed to mycobacterial cell wall lipoarabinomannan become highly susceptible to HIV-1 [48].…”

Section: Discussionmentioning

confidence: 97%

Human immunodeficiency virus type-1 group M quasispecies evolution: diversity and divergence in patients co-infected with active tuberculosis

Biru

Lennemann

Stürmer

et al. 2010

Med Microbiol Immunol

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The evolution of intra-host human immunodeficiency virus type 1 (HIV-1) quasispecies prior and after treating active tuberculosis (TB) with chemotherapy in HIV-1/TB patients was assessed. Two time points HIV-1 quasispecies were evaluated by comparing HIV-1-infected patients with active tuberculosis (HIV-1/TB) and HIV-1-infected patients without tuberculosis (HIV-1/non-TB). Plasma samples were obtained from the Frankfurt HIV cohort, and HIV-1 RNA was isolated. C2V5 env was amplified by PCR and molecular cloning was performed. Eight to twenty-five clones were sequenced from each patient. Various phylogenetic analyses were performed. We found a significant increase in diversity and divergence in HIV-1/TB compared to the HIV-1/non-TB. For HIV-1/TB, the average rate of evolution of C2V5 env was higher than previous reports (2.4 × 10(-4) substitution/site/day). Two groups of HIV-1/TB were observed based on the rate of HIV-1 evolution and coreceptor usage: A fast evolving R5-tropic dominating group and a relatively slowly evolving X4 group. The results demonstrated that active TB has an impact on HIV-1 viral diversity and divergence over time. The influence of active TB on longitudinal evolution of HIV-1 may be predominant for R5 viruses.

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“…Of note, levels of expression of CCR2, the receptor for MCP‐1, on macrophages in PFMC far exceeded that on T‐cells. Whether this indicates a predominant effect of MCP‐1 on transcriptional activation of HIV‐1 in macrophages at sites of MTB infection needs to be addressed considering the extremely high levels of this chemokine in pleural fluid, and with recent data confirming macrophages as a source for HIV‐1 at sites of HIV/TB infection [20, 21] .…”

Section: Discussionmentioning

confidence: 99%

The Interaction of Monocyte Chemoattractant Protein‐1 and Tumour Necrosis Factor‐α in Mycobacterium tuberculosis‐induced HIV‐1 Replication at Sites of Active Tuberculosis

Mayanja‐Kizza

Aung

et al. 2009

Scand J Immunol

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Tuberculosis (TB) is a prominent opportunistic infection in HIV‐1‐infected subjects and enhances HIV‐1 replication. TB is associated with excess monocyte chemoattractant protein (MCP)‐1 and tumour necrosis factor (TNF)‐α activity in situ, both of which are implicated in transcriptional activation of HIV‐1. The role of MCP‐1 and TNF‐α in activation of HIV‐1 during TB and by Mycobacterium tuberculosis (MTB) in mononuclear cells from HIV‐1/TB subjects with pleural TB was examined here. Extremely high levels of MCP‐1 (as compared with TNF‐α) protein and mRNA were found in pleural fluid and pleural fluid mononuclear cells. Levels of MCP‐1 mRNA were sustained during in vitro culture of pleural fluid mononuclear cells. Neutralization of MCP‐1 (but not TNF‐α), resulted in inhibition of MTB induced HIV‐1 gag/pol mRNA. Neutralization of both MCP‐1 and TNF‐α, however, abrogated the effect of anti‐MCP‐1 antibody on HIV‐1 mRNA. LMP‐420, a small molecular transcriptional inhibitor of both TNF‐α and MCP‐1 expression, did not reduce MTB‐induced HIV‐1 expression. These data imply that MCP‐1 activity may be critical to activation of HIV‐1 at sites of TB. An interplay of MCP‐1 and TNF‐α is also suggested.

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Mycobacterium tuberculosis-induced CXCR4 and chemokine expression leads to preferential X4 HIV-1 replication in human macrophages

Abstract: tuberculosis-induced CXCR4 and chemokine expression leads to preferential X4 HIV-1 replication in human macrophages.

Cited by 15 publications

References 0 publications

Mechanisms of Polymorphonuclear Neutrophil–Mediated Induction of HIV‐1 Replication in Macrophages during Pulmonary Tuberculosis

Mechanisms of Polymorphonuclear Neutrophil–Mediated Induction of HIV‐1 Replication in Macrophages during Pulmonary Tuberculosis

Human immunodeficiency virus type-1 group M quasispecies evolution: diversity and divergence in patients co-infected with active tuberculosis

The Interaction of Monocyte Chemoattractant Protein‐1 and Tumour Necrosis Factor‐α in Mycobacterium tuberculosis‐induced HIV‐1 Replication at Sites of Active Tuberculosis

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