Important note: Information in this article was accurate in April 2000. The state of the art may have changed since the publication date.AIDSWEEKLY Plus; Monday, April 3, 2000
Prepared by AIDS Weekly editors from staff and other reports
This suggestion was made based on a study conducted by A. Yenmoore et al. and reported in Virology ("Differential expression of the HHV-8 vGCR cellular homolog gene in AIDS-associated and classic Kaposi's sarcoma: Potential role of HIV-1 Tat," Virology 2000 Feb 15;267(2):247-51
Study authors said, "There is significant homology between some HHV-8 genes and cellular genes including D-type cyclin (vCYC), G protein coupled receptor (vGCR), macrophage inflammatory proteins (vMIP-I, vMIP-II), bcl-2 (vBCL2), interferon regulatory factor-1 (vIRF1), interleukin-6 (vIL6), and complement binding protein (vCBP)."
They analyzed the expression of these viral homologs and HIV-1 using standard analytical methods in various tissue and cell types. AIDS-KS (AKS) tissue, classic KS tissue (CKS), peripheral blood mononuclear cells (PBMC), and both phorbol ester (TPA)-treated and untreated HHV-8 positive lymphoma cells (BCBL1) were analyzed.
Yenmoore et al. found that vCYC, vMIP-I, vBCL2, and vIRF1 transcripts could be detected in AKS and CKS.
However, vGCR and HIV-1 Tat were only expressed in AKS samples, Yenmoore and colleagues reported.
No KS samples showed evidence of vMIP-II, vCBP, and vIL6 expression, they also reported.
They concluded, "Since vGCR expression is limited to AKS, it is possible that vGCR is activated by HIV-1 Tat. These results suggest that HIV-1 Tat may contribute to AKS pathogenesis through the tumorigenic and angiogenic effects of vGCR."
To see 10 additional articles relating to both HHV-8 and Kaposi's sarcoma, visit www.NewsRx.com.
The corresponding author for this study is S.K. Tyring, University of Texas, Medical Branch, Department of Dermatology, Route 1070, Galveston, TX 77555, USA.
Key points reported in this study are:
This article was prepared by AIDS Weekly editors from staff and other reports.
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