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  4. Reciprocal Regulatory Interaction between Human Herpesvirus 8 and Human Immunodeficiency Virus Type 1
 
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Reciprocal Regulatory Interaction between Human Herpesvirus 8 and Human Immunodeficiency Virus Type 1

Journal
Journal of Biological Chemistry
Journal Volume
276
Journal Issue
16
Pages
13427-13432
Date Issued
2001
Author(s)
LI-MIN HUANG  
Chao M.-F.
Chen M.-Y.
Shih H.-M.
Chiang Y.-P.
Chuang C.-Y.
Lee C.-Y.
DOI
10.1074/jbc.M011314200
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-0035918324&doi=10.1074%2fjbc.M011314200&partnerID=40&md5=52b4c3b99e5899c0b8329ba5b5d7a89f
https://scholars.lib.ntu.edu.tw/handle/123456789/566670
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 HHVS-specific expression. These results provide molecular insights correlating coinfection with HHV8 and HIV-1 with an unusually high incidence of KS.
SDGs

[SDGs]SDG3

Other Subjects
Genes; Immunology; Pathology; HIV infection; Pathogenesis; Viruses; transactivator protein; Vpr protein; ribonuclease; article; cancer incidence; comorbidity; controlled study; correlation analysis; gene expression regulation; host; human; human cell; Human herpesvirus 8; Human immunodeficiency virus 1; Human immunodeficiency virus infection; Kaposi sarcoma; long terminal repeat; prevalence; priority journal; upregulation; acquired immune deficiency syndrome; cell fusion; cell line; genetic transfection; genetics; HeLa cell; homeostasis; Kaposi sarcoma; leukemia cell line; metabolism; pathophysiology; physiology; promoter region; reverse transcription polymerase chain reaction; virology; DNA viruses; Herpesviridae; Human herpesvirus 8; Human immunodeficiency virus; Human immunodeficiency virus 1; RNA viruses; herpesvirus 8; Acquired Immunodeficiency Syndrome; Cell Fusion; Cell Line; Gene Products, tat; Hela Cells; Herpesvirus 8, Human; HIV Long Terminal Repeat; HIV-1; Homeostasis; Humans; Jurkat Cells; Promoter Regions (Genetics); Reverse Transcriptase Polymerase Chain Reaction; Ribonucleases; Sarcoma, Kaposi; Transfection
Type
journal article

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