Infection with human T-lymphotropic viras type III and leukocyte interferon production in homosexual men

J, Abb; Piechowiak, H; Zachoval, Reinhart; Zachoval, Vera; Deinhardt, Friedrich

doi:10.1007/bf02017803

Cited by 11 publications

(4 citation statements)

References 8 publications

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“…Transcription of the IFN-,y gene, but not the ILr2 gene, is impaired in HIV-infected T cells (40). Similarly, monocytes and PBMC from HIV-infected patients show a markedly reduced ability to secrete IFN-ci or express IFN-a mRNA after exposure to vesicular stomatitis virus, influenza A virus, or HSV type 1 infected fibroblasts (41)(42)(43) . What is most remarkable about these latter observations, is that they occur coincident with a frequency of HIV-infected cells in patient blood that is exceedingly low.…”

Section: Discussionmentioning

confidence: 99%

A selective defect of interferon alpha production in human immunodeficiency virus-infected monocytes.

Gendelman

Friedman

Joe

et al. 1990

The Journal of Experimental Medicine

132

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Interferon alpha (IFN-alpha) induces significant antiretroviral activities that affect the ability of human immunodeficiency virus (HIV) to infect and replicate in its principal target cells, CD4+ T cells and macrophages. A major endogenous source of IFN-alpha during any infection is the macrophage. Thus, macrophages have the potential to produce both IFN-alpha and HIV. In this study, we examined the production of IFN-alpha and other cytokines by macrophage colony-stimulating factor (M-CSF)-treated cultured monocytes during HIV infection. Tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), IL-6, IFN-omega, or IFN-beta were not detected nor was the mRNA expressed in either uninfected or HIV-infected monocytes. However, both uninfected and HIV-infected monocytes produced high levels of each of these cytokines after treatment with synthetic double-stranded RNA [poly(I).poly(C)]. Uninfected monocytes also produced high levels of IFN-alpha after treatment with poly(I).poly(C), Newcastle disease virus, or herpes simplex virus. In marked contrast to the preceding observations, HIV-infected monocytes produced little or no IFN-alpha before or after treatment with any of these agents. The absence of detectable IFN-alpha activity and mRNA in poly(I).poly(C)-treated HIV-infected monocytes was coincident with high levels of 2',5' oligoadenylate synthetase and complete ablation of HIV gene expression. The antiviral activity induced by poly(I).poly(C) may be a direct effect of this synthetic double-stranded RNA or secondary to the low levels of IFN-beta and IFN-omega produced by infected cells. The markedly diminished capacity of HIV-infected monocytes to produce IFN-alpha may reflect a specific adaptive mechanism of virus to alter basic microbicidal functions of this cell. The inevitable result of this HIV-induced cytokine dysregulation is virus replication and persistence in mononuclear phagocytes.

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Section: Discussionmentioning

confidence: 99%

A selective defect of interferon alpha production in human immunodeficiency virus-infected monocytes.

Gendelman

Friedman

Joe

et al. 1990

The Journal of Experimental Medicine

132

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“…During HIV-1 infection, the primary stage is associated with a transient IFN-x response [20]. and IFN-a then reappears in the circulation at increasing levels during progression of the disease [20][21][22]. The increased serum levels of IFN-a are not parallelled by increased ability of blood leucocytes to produce IFN-a upon stimulation by inducing agents: rather this ability successively diminishes as the disease progresses [22].…”

Section: Introductionmentioning

confidence: 99%

Raised levels of tumour necrosis factor-alpha and neopterin, but not interferon-alpha, in serum of HIV-1-infected patients from Ethiopia

Ayehunie

Sönnerborg²,

Yemane-Berhan

et al. 1993

Clinical and Experimental Immunology

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SUMMARY Serum levels of tumour necrosis factor‐alpha (TNF‐α). neopterin and interferon‐alpha (IFN‐α) were determined by immunoradiometric assays in 60 HIV‐1+and 20 HIV‐1− subjects from Ethiopia. Swedish samples were used as reference material. The Ethiopian HIV‐1‘ subjects were found to have significantly increased TNF‐α and neopterin, but not IFN‐α levels. Increased levels of TNF‐α and neopterin were frequently found in Ethiopian asymptomatic subjects (37% and 41%). and the concentration increased in patients with AIDS (83% and 90% respectively). The levels of the two substances and the proportion of patients with higher TNF‐α values were lower in the corresponding Swedish subjects. The proportion of sera with raised levels of I FN‐α was very low (asymptomatic 4%, and AIDS 7%) in Ethiopian subjects. These results suggest a very early increase in the TNF‐α production and activation of the cellular immune response, and a low level of IFN‐α synthesis in the natural course of HIV infection in Ethiopia. The aberrations may contribute to a rapid progress of immunodeficiency and cachexia often seen in Ethiopian patients.

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“…Production of IFN-y by peripheralblood mononuclear cells (PBMC) of HIV-infected pa tients is significantly reduced [16]. Transcription of the IFN-y gene, but not the IL-2 gene, is impaired in HIVinfected T cells [17], Similarly, monocytes and PMBC from HIV-infected patients show a markedly reduced ability to secrete IFN-a or express IFN-a mRNA after exposure to vesicular stomatitis virus, influenza A virus or herpes virus type 1 infected fibroblasts [18][19][20]. The mechanism for the transcriptional block in IFN-a gene expression is not yet known.…”

mentioning

confidence: 99%

Regulation of Cytokine and Viral Gene Expression in Monocytes Infected with the Human Immunodeficiency Virus

et al. 1991

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Monocytes treated with interferon-α (IFN-α) at virus challenge show no evidence of human immunodeficiency virus (HIV) infection: no p24 antigen or reverse transcriptase (RT) activity, no viral mRNA and no proviral DNA. Levels of p24 antigen and RT activity in monocytes infected with HIV 1–3 weeks before IFN-α treatment gradually decrease to baseline. HIV-induced cytopathic changes are markedly reduced, as are levels of HIV mRNA: the frequency of productively infected cells is ≤ 1 %. But, levels of proviral DNA in the IFN-α-treated and control HIV-infected cells are indistinguishable, and remain so through 3 weeks. Large quantities of proviral DNA in IFN-α-treated cells with little active transcription suggest true microbiological latency. The major potential source for IFN-α in HIV-infected patients is the macrophage. With any of 15 virus isolates, tumor necrosis factor-α, interleukin-1 β, interleukin-6, IFN-ω or IFN-β are not detected nor the mRNA expressed in HIV-infected or uninfected monocytes. Both uninfected and HIV-infected monocytes produce high levels of these cytokines after treatment with synthetic double-stranded RNA (poly-LC). Uninfected monocytes also produce high levels of IFN-α after treatment with Poly-I:C, Newcastle disease virus or herpes simplex virus. In marked contrast, HIV-infected monocytes express no IFN-α activity or mRNA before or after treatment with any of these agents. The markedly diminished capacity of HIV-infected monocyte to produce IFN-α reflects a specific transcriptional block and may be an adaptive mechanism of virus to alter basic microbicidal functions of this cell. The inevitable result of this HIV-induced cytokine dysregulation is virus replication and persistence in mononuclear phagocytes.

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Infection with human T-lymphotropic viras type III and leukocyte interferon production in homosexual men

Cited by 11 publications

References 8 publications

A selective defect of interferon alpha production in human immunodeficiency virus-infected monocytes.

A selective defect of interferon alpha production in human immunodeficiency virus-infected monocytes.

Raised levels of tumour necrosis factor-alpha and neopterin, but not interferon-alpha, in serum of HIV-1-infected patients from Ethiopia

Regulation of Cytokine and Viral Gene Expression in Monocytes Infected with the Human Immunodeficiency Virus

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