摘要
Hepatitis B virus(HBV) and hepatitis C virus(HCV) infections are the most common causes of chronic liver diseases and hepatocelluar carcinomas. Over the past few years, the liver-enriched micro RNA-122(mi R-122) has been shown to differentially regulate viral replication of HBV and HCV. It is notable that thelevel of mi R-122 is positively and negatively regulated by HCV and HBV, respectively. Consistent with the welldocumented phenomenon that mi R-122 promotes HCV accumulation, inhibition of mi R-122 has been shown as an effective therapy for the treatment of HCV infection in both chimpanzees and humans. On the other hand, mi R-122 is also known to block HBV replication, and HBV has recently been shown to inhibit mi R-122 expression; such a reciprocal inhibition between mi R-122 and HBV suggests an intriguing possibility that mi R-122 replacement may represent a potential therapy for treatment of HBV infection. As HBV and HCV have shared transmission routes, dual infection is not an uncommon scenario, which is associated with more advanced liver disease than either HBV or HCV mono-infection. Thus, there is a clear need to further understand the interaction between HBV and HCV and to delineate the role of mi R-122 in HBV/HCV dual infection in order to devise effective therapy. This review summarizes the current understanding of HBV/HCV dual infection, focusing on the pathobiological role and therapeutic potential of mi R-122.
Hepatitis B virus （HBV） and hepatitis C virus （HCV）infections are the most common causes of chronicliver diseases and hepatocelluar carcinomas. Overthe past few years, the liver-enriched microRNA-122（miR-122） has been shown to differentially regulateviral replication of HBV and HCV. It is notable that thelevel of miR-122 is positively and negatively regulatedby HCV and HBV, respectively. Consistent with the welldocumentedphenomenon that miR-122 promotes HCVaccumulation, inhibition of miR-122 has been shown asan effective therapy for the treatment of HCV infectionin both chimpanzees and humans. On the other hand,miR-122 is also known to block HBV replication, andHBV has recently been shown to inhibit miR-122expression; such a reciprocal inhibition betweenmiR-122 and HBV suggests an intriguing possibilitythat miR-122 replacement may represent a potentialtherapy for treatment of HBV infection. As HBV andHCV have shared transmission routes, dual infection isnot an uncommon scenario, which is associated withmore advanced liver disease than either HBV or HCVmono-infection. Thus, there is a clear need to furtherunderstand the interaction between HBV and HCVand to delineate the role of miR-122 in HBV/HCV dualinfection in order to devise effective therapy. This reviewsummarizes the current understanding of HBV/HCVdual infection, focusing on the pathobiological role andtherapeutic potential of miR-122.
基金
Supported by Grants from NIDDK and NCI
