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Logo of bmcimmBioMed Centralsearchsubmit a manuscriptregisterthis articleBMC Immunology
 
BMC Immunol. 2012; 13: 15.
Published online Apr 3, 2012. doi:  10.1186/1471-2172-13-15
PMCID: PMC3350415
The Tat protein of human immunodeficiency virus-1 enhances hepatitis C virus replication through interferon gamma-inducible protein-10
Jing Qu,1 Qi Zhang,1 Youxing Li,1 Weiyong Liu,1 Lvxiao Chen,1 Ying Zhu,1,2 and Jianguo Wucorresponding author1,2,3
1State Key Laboratory of Virology, College of Life Sciences, and Chinese-French Liver Disease Research Institute at Zhongnan Hospital, Wuhan University, Wuhan 430072, P.R. China
2Wuhan Institutes of Biotechnology, 666 Gaoxin Road, Wuhan East Lake High Technology Development Zone, Wuhan 430075, P.R. China
3State Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China
corresponding authorCorresponding author.
Jing Qu: jingqu2006/at/yahoo.com.cn; Qi Zhang: ciceling/at/yahoo.com.cn; Youxing Li: lyx1031/at/163.com; Weiyong Liu: weiyongliu/at/gmail.com; Lvxiao Chen: wu9988/at/vip.sina.com; Ying Zhu: yingzhu/at/whu.edu.cn; Jianguo Wu: jwu/at/whu.edu.cn
Received November 13, 2011; Accepted April 3, 2012.
Abstract
Background
Co-infection with human immunodeficiency virus-1 (HIV-1) and hepatitis C virus (HCV) is associated with faster progression of liver disease and an increase in HCV persistence. However, the mechanism by which HIV-1 accelerates the progression of HCV liver disease remains unknown.
Results
HIV-1/HCV co-infection is associated with increased expression of interferon gamma-induced protein-10 (IP-10) mRNA in peripheral blood mononuclear cells (PBMCs). HCV RNA levels were higher in PBMCs of patients with HIV-1/HCV co-infection than in patients with HCV mono-infection. HIV-1 Tat and IP-10 activated HCV replication in a time-dependent manner, and HIV-1 Tat induced IP-10 production. In addition, the effect of HIV-1 Tat on HCV replication was blocked by anti-IP-10 monoclonal antibody, demonstrating that the effect of HIV-1 Tat on HCV replication depends on IP-10. Taken together, these results suggest that HIV-1 Tat protein activates HCV replication by upregulating IP-10 production.
Conclusions
HIV-1/HCV co-infection is associated with increased expression of IP-10 mRNA and replication of HCV RNA. Furthermore, both HIV-1 Tat and IP-10 activate HCV replication. HIV-1 Tat activates HCV replication by upregulating IP-10 production. These results expand our understanding of HIV-1 in HCV replication and the mechanism involved in the regulation of HCV replication mediated by HIV-1 during co-infection.
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