國家衛生研究院 NHRI:Item 3990099045/2171
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/2171


    Title: Reciprocal regulatory interaction between human herpesvirus 8 and human immunodeficiency virus type 1
    Authors: Huang, LM;Chao, MF;Chen, MY;Shih, HM;Chiang, YP;Chuang, CY;Lee, CY
    Contributors: Division of Molecular and Genomic Medicine
    Abstract: Human herpesvirus 8 (HHV8) is the primary viral etiologic agent in Kaposi's sarcoma (KS). However, individuals dually infected with both HHV8 and human immunodeficiency virus type 1 (HIV-1) show an enhanced prevalence of KS when compared with those singularly infected with HHV8. Host immune suppression conferred by HIV infection cannot wholly explain this increased presentation of KS. To better understand how HHV8 and HIV 1 might interact directly in the pathogenesis of KS, we queried for potential regulatory interactions between the two viruses. Here, we report that HHV8 and HIV-1 reciprocally up-regulate the gene expression of each other. We found that the KIE2 immediate-early gene product of HHV8 interacted synergistically with Tat in activating expression from the HIV-1 long terminal repeat. On the other hand, HIV-1 encoded Tat and Vpr proteins increased intracellular HHV8-specific expression. These results provide molecular insights correlating coinfection with HHV8 and HIV-1 with an unusually high incidence of KS.
    Keywords: Biochemistry & Molecular Biology
    Date: 2001-04-20
    Relation: Journal of Biological Chemistry. 2001 Apr;276(16):13427-13432.
    Link to: http://dx.doi.org/10.1074/jbc.M011314200
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1083-351X&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000168198600131
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0035918324
    Appears in Collections:[Hsiu-Ming Shih] Periodical Articles

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