AZT blocks down-regulation of IL-2 and IFN-γ gene expression in HIV acutely infected cells

AZT blocks down-regulation of IL-2 and IFN-γ gene expression in HIV acutely infected cells HIV infection causes dysregulation of cytokine gene expression in CD4 + T cells of the infected host. Azidothymidine (AZT) inhibits HIV repli-cation by blocking reverse transcription. Using a one-stop cell-to-cell HIV infection model, we have investigated the expression of several key cytokines in HIV infected T cells in the absence or presence of AZT treatment. Acute HIV infection of T cells resulted in dramatic down regulation of the expression of IL-2 and INFg mRNA. While β-actin mRNA levels remained constant in both AZT-free and AZT treated cultures after HIV infection, it was found that AZT blocked the down regulation of IL-2 mRNA and INFg mRNA in CD4 + T cells acutely infected with HIV. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

AZT blocks down-regulation of IL-2 and IFN-γ gene expression in HIV acutely infected cells

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Publisher
Springer Journals
Copyright
Copyright © Wien by 1997 Springer-Verlag/
Subject
Legacy
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s007050050139
Publisher site
See Article on Publisher Site

Abstract

HIV infection causes dysregulation of cytokine gene expression in CD4 + T cells of the infected host. Azidothymidine (AZT) inhibits HIV repli-cation by blocking reverse transcription. Using a one-stop cell-to-cell HIV infection model, we have investigated the expression of several key cytokines in HIV infected T cells in the absence or presence of AZT treatment. Acute HIV infection of T cells resulted in dramatic down regulation of the expression of IL-2 and INFg mRNA. While β-actin mRNA levels remained constant in both AZT-free and AZT treated cultures after HIV infection, it was found that AZT blocked the down regulation of IL-2 mRNA and INFg mRNA in CD4 + T cells acutely infected with HIV.

Journal

Archives of VirologySpringer Journals

Published: May 1, 1997

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