Cytokines Alter Production of HIV-1 from Primary Mononuclear Phagocytes

Koyanagi, Yoshio; O’Brien, William A.; Zhao, Jia; Golde, David W.; Gasson, Judith C.; Chen, Irvin S. Y.

doi:10.1126/science.3047875

Cited by 459 publications

(185 citation statements)

References 36 publications

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“…M. tuberculosis up-regulates the genes for these cytokines in peripheral blood monocytes (PBM)1 in vivo from patients with active tuberculosis, and release of these cytokines is enhanced when these cells are cultured in vitro (23,24). These cytokines enhance replication of HIV-1 in vitro using several cell lines (25). The mechanism of this stimulation has been localized to the 5' long terminal repeat (LTR) of HIV-1, and specifically to the nuclear factor (NF)-KB transcription enhancer site (26)(27)(28)(29)(30)(31)(32) (33).…”

Section: -263-8442mentioning

confidence: 99%

Mycobacterium tuberculosis enhances human immunodeficiency virus-1 replication by transcriptional activation at the long terminal repeat.

Zhang

Nakata²,

Weiden³

et al. 1995

J. Clin. Invest.

169

108

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construct, live M. tuberculosis increased transcription 20-fold in THP-1 cells, and cell wall components stimulated CAT expression to a lesser extent. The nuclear factor-KB enhancer element was responsible for the majority of the increased CAT activity although two upstream nuclear factor-IL6 sites may also contribute to enhanced transcription. Antibodies to TNF-a and IL-1 inhibited the increase in CAT activity of the HIV-1 long terminal repeat by M. tuberculosis from 21-fold to 8-fold. Stimulation of HIV-1 replication by M. tuberculosis may exacerbate dysfunction of the host immune response in dually infected individuals. (J. Clin. Invest. 1995Invest. . 95:2324Invest. -2331

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Section: -263-8442mentioning

confidence: 99%

Mycobacterium tuberculosis enhances human immunodeficiency virus-1 replication by transcriptional activation at the long terminal repeat.

Zhang

Nakata²,

Weiden³

et al. 1995

J. Clin. Invest.

169

108

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“…Since it has been shown that cytokines may alter the production of HIV 1 in primary mononuclear phagocytes (Koyanagi et al, 1988}, microglial cells were kept beside GM-CSF also in the presence of 11-1 , and 11-3. However, none of these cytokines changed significantly either the virus replication kinetics or virus yield.…”

Section: Phenotypic Characterization Of Isolated Microglial Cellsmentioning

confidence: 99%

In Vitro and in Vivo Infection of Rhesus Monkey Microglial Cells by Simian Immunodeficiency Virus

et al. 1993

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The observation that microglial cells in brain tissue are probably a major target for human immunodeficiency virus (HIV) infection has raised interest in the pathogenic role of this cell population for the development of neuro-AIOS.Since it is very difficult to obtain microglia from normal or diseased human brain we studied microglial cells isolated from fresh brain tissue of uninfected and simian immunodeficiency virus (SIV) infected rhesus monkeys (Macacca mulatta) in comparison to peripheral blood macrophages. Besides the characterization of the phenotypes of these two cell populations, we examined the replication of SIV in the cells in addition to the effect of viral infection on the expression of cell surface molecules. We found that microglia and macrophages support replication of the wild-type S1Vmac 25 , strain as weil as the infectious clone (SIV 239 ). lnfectious viruswas produced and a CPE developed. lsolated microglial cells from SIV-infected monkeys were latently infected independent of the presence of neuropathological lesions and produced infectious virus after 20-25 days in culture. ln situ hybridization revealed that only a small percentage of isolated microglial cells are productively infected in vivo, yet the majority of these expressed MHC class II molecules. This indicated a state of activation that is acquired in vivo. These findings indicate that microglia are a prime target cell for SIV infection in CNS tissue.

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“…Primary T cells and MDMs used in the preceding studies were cultured in the presence of interleukin 2 (20 U/ml) and phytohemagglutinin (PHA, 2.5 g/ ml) or granulocyte-macrophage colony-stimulating factor (GM-CSF, 40 U/ml) and M-CSF (M-CSF, 100 U/ml), respectively. In studies of HIV-1 infection, these extracellular factors have been used to activate primary immune cells and enhance viral replication (19). To determine if cytokine stimulation influenced primary cell sensitivity to microbicide exposure and affected the comparisons between cell lines and primary cells, SupT1 and U-937 cells were cultured under conditions identical to those for their respective primary cell counterparts and were assessed for microbicide sensitivity after a 10-min or 48-h exposure (Fig.…”

mentioning

confidence: 99%

Comparative In Vitro Sensitivities of Human Immune Cell Lines, Vaginal and Cervical Epithelial Cell Lines, and Primary Cells to Candidate Microbicides Nonoxynol 9, C31G, and Sodium Dodecyl Sulfate

Krebs

Miller

Catalone

et al. 2002

Antimicrob Agents Chemother

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In experiments to assess the in vitro impact of the candidate microbicides nonoxynol 9 (N-9), C31G, and sodium dodecyl sulfate (SDS) on human immune and epithelial cell viability, cell lines and primary cell populations of lymphocytic and monocytic origin were generally shown to be equally sensitive to exposures ranging from 10 min to 48 h. However, U-937 cells were more sensitive to N-9 and C31G after 48 h than were primary monocyte-derived macrophages. Cytokine activation of monocytes and lymphocytes had no effect on cell viability following exposure to these microbicidal compounds. Primary and passaged vaginal epithelial cultures and cell lines differed in sensitivity to N-9 and C31G but not SDS. These studies provide a foundation for in vitro experiments in which cell lines of human immune and epithelial origin can be used as suitable surrogates for primary cells to further investigate the effects of microbicides on cell metabolism, membrane composition, and integrity and the effects of cell type, proliferation, and differentiation on microbicide sensitivity.

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Cytokines Alter Production of HIV-1 from Primary Mononuclear Phagocytes

Cited by 459 publications

References 36 publications

Mycobacterium tuberculosis enhances human immunodeficiency virus-1 replication by transcriptional activation at the long terminal repeat.

Mycobacterium tuberculosis enhances human immunodeficiency virus-1 replication by transcriptional activation at the long terminal repeat.

In Vitro and in Vivo Infection of Rhesus Monkey Microglial Cells by Simian Immunodeficiency Virus

Comparative In Vitro Sensitivities of Human Immune Cell Lines, Vaginal and Cervical Epithelial Cell Lines, and Primary Cells to Candidate Microbicides Nonoxynol 9, C31G, and Sodium Dodecyl Sulfate

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