TY - JOUR
T1 - Differential expression of the HHV-8 vGCR cellular homolog gene in AIDS- associated and classic kaposrs sarcoma
T2 - Potential role of HIV-1 tat
AU - Yen-Moore, Angela
AU - Hudnall, S. David
AU - Rady, Peter L.
AU - Wagner, Richard F.
AU - Moore, Todd O.
AU - Memar, Omeed
AU - Hughes, Thomas K.
AU - Tyring, Stephen K.
PY - 2000/2/15
Y1 - 2000/2/15
N2 - Human herpesvirus 8 (HHV-8) has been causally linked to Kaposi's sarcoma (KS). 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-l, vMIP-11), bcl-2 (vBCL2), interferon regulatory factor-1 (vlRF1), interleukin-6 (vlL6), and complement-binding protein (vCBP). In this study, we analyzed expression of these viral homologs and HIV-1 Tat by reverse transcriptase polymerase chain reaction (RT-PCR) coupled with Southern blot hybridization in AIDS-KS (AKS) tissue, classic KS tissue(CKS), and peripheral blood mononuclear cells, and phorbol ester (TPA)- treated and untreated HHV-8 positive lymphoma cells (BCBL1). While vCYC (AKS 6 of 6; CKS 3 of 3), vMIP-l (AKS 5 of 6, CKS 3 of 3), vBCL2 (AKS 6 of 6; CKS 3 of 3), and vlRF1 (AKS 5 of 6, CKS 3 of 3) transcripts were detected in both AKS and CKS, vGCR and HIV-1 Tat were expressed only in AKS samples (vGCR: AKS 3 of 6, CKS 0 of 3; Tat: AKS 4 of 6, CKS 0 of 3). vMlPII, vCBP, and vlL6 expression were not detected in any KS samples. 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. (C) 2000 Academic Press.
AB - Human herpesvirus 8 (HHV-8) has been causally linked to Kaposi's sarcoma (KS). 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-l, vMIP-11), bcl-2 (vBCL2), interferon regulatory factor-1 (vlRF1), interleukin-6 (vlL6), and complement-binding protein (vCBP). In this study, we analyzed expression of these viral homologs and HIV-1 Tat by reverse transcriptase polymerase chain reaction (RT-PCR) coupled with Southern blot hybridization in AIDS-KS (AKS) tissue, classic KS tissue(CKS), and peripheral blood mononuclear cells, and phorbol ester (TPA)- treated and untreated HHV-8 positive lymphoma cells (BCBL1). While vCYC (AKS 6 of 6; CKS 3 of 3), vMIP-l (AKS 5 of 6, CKS 3 of 3), vBCL2 (AKS 6 of 6; CKS 3 of 3), and vlRF1 (AKS 5 of 6, CKS 3 of 3) transcripts were detected in both AKS and CKS, vGCR and HIV-1 Tat were expressed only in AKS samples (vGCR: AKS 3 of 6, CKS 0 of 3; Tat: AKS 4 of 6, CKS 0 of 3). vMlPII, vCBP, and vlL6 expression were not detected in any KS samples. 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. (C) 2000 Academic Press.
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U2 - 10.1006/viro.1999.0125
DO - 10.1006/viro.1999.0125
M3 - Article
C2 - 10662620
AN - SCOPUS:0034652396
SN - 0042-6822
VL - 267
SP - 247
EP - 251
JO - Virology
JF - Virology
IS - 2
ER -