Hepatitis B virus/hepatitis C virus coinfection: Epidemiology, clinical features, viral interactions and treatment
Article first published online: 3 APR 2008
© 2008 The Authors
Journal of Gastroenterology and Hepatology
Volume 23, Issue 4, pages 512–520, April 2008
How to Cite
Chu, C.-J. and Lee, S.-D. (2008), Hepatitis B virus/hepatitis C virus coinfection: Epidemiology, clinical features, viral interactions and treatment. Journal of Gastroenterology and Hepatology, 23: 512–520. doi: 10.1111/j.1440-1746.2008.05384.x
- Issue published online: 3 APR 2008
- Article first published online: 3 APR 2008
- Accepted for publication 8 January 2008.
- hepatitis B virus;
- hepatitis C virus;
- hepatocellular carcinoma;
- pegylated interferon;
- sustained virological response
Because of the shared modes of transmission, hepatitis B virus (HBV)/hepatitis C virus (HCV) coinfection is not uncommon in highly endemic areas and among subjects with a high risk of parenteral infections. The worldwide prevalence of HBV/HCV coinfection is unknown and might be underestimated with the phenomenon of silent (occult) HBV infection. HCV superinfection in patients with chronic HBV infection was the most common clinical features of coinfection in Asia–Pacific countries. Further, most, but not all, clinical observations suggested that interference between the two viruses was more frequently characterized by an inhibition of HBV replication exerted by HCV. However, longitudinal follow-up studies have demonstrated that the virological patterns in coinfection cases are widely divergent and have dynamic profiles over time. As compared with monoinfected patients, HBV/HCV coinfected persons tend to have more severe liver injury, a higher probability of liver cirrhosis and hepatic decompensation, and a higher incidence of hepatocellular carcinoma. Detailed serological and virological evaluations are required for coinfected patients before initiation of antiviral therapy. Previous studies demonstrated that HBV/HCV coinfected patients responded poorly to interferon (IFN) monotherapy. Currently, for patients with dominant HCV infection and low level HBV viremia (<104 IU/mL), IFN or pegylated IFN plus ribavirin can achieve comparable sustained virus response as expected with HCV monoinfection. However, phenomenon of reciprocal viral interference can happen, and resultant “flare” of hepatitis activity may cause liver function deterioration. For coinfected patients with dually-active HBV/HCV, the optimal regimen for therapy remains unclear although adding oral nucleos(t)ide analogs to pegylated IFN and ribavirin seems a reasonable empiric option.