April 3, 2012

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

Published on: 2012-04-03

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.Please see related article: http://www.biomedcentral.com/1741-7015/10/32

Author: Jing QuQi ZhangYouxing LiWeiyong LiuLvxiao ChenYing ZhuJianguo Wu

Credits/Source: BMC Immunology 2012, 13:15

Source

No comments:

Post a Comment