The Tat protein of human immunodeficiency virus-1 enhances hepatitis C virus replication through interferon gamma-inducible protein-10

被引:24
作者
Qu, Jing [1 ,2 ]
Zhang, Qi [1 ,2 ]
Li, Youxing [1 ,2 ]
Liu, Weiyong [1 ,2 ]
Chen, Lvxiao [1 ,2 ]
Zhu, Ying [1 ,2 ,3 ]
Wu, Jianguo [1 ,2 ,3 ,4 ,5 ]
机构
[1] Wuhan Univ, Zhongnan Hosp, Coll Life Sci, State Key Lab Virol, Wuhan 430072, Peoples R China
[2] Wuhan Univ, Zhongnan Hosp, Chinese French Liver Dis Res Inst, Wuhan 430072, Peoples R China
[3] Wuhan Inst Biotechnol, Wuhan 430075, Peoples R China
[4] Wuhan Univ, State Key Lab Virol, Wuhan 430072, Peoples R China
[5] Wuhan Univ, Coll Life Sci, Wuhan 430072, Peoples R China
基金
中国国家自然科学基金;
关键词
ACTIVE ANTIRETROVIRAL THERAPY; PERIPHERAL-BLOOD MONOCYTES; HIV-INFECTION; TYPE-1; TAT; FIBROSIS PROGRESSION; MESSENGER-RNA; LIVER-DISEASE; JC VIRUS; IP-10; CHEMOKINE;
D O I
10.1186/1471-2172-13-15
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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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页数:12
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