Clin Res Hepatol Gastroenterol. 2013 Feb;37(1):e16-20.

Hepatitis B virus and hepatitis C virus co-infection: a therapeutic challenge.

Hamzaoui L, El Bouchtili S, Siai K, Mahmoudi M, Azzouz MM.

Gastroenterology department, Mohamed Tahar Maamouri Hospital, Nabeul, Tunisia.



Hepatitis B virus and hepatitis C virus are the two most common causes of chronic liver disease in the world. Dual infection with hepatitis B virus and hepatitis C virus, whose prevalence is underestimated, is characterized by a more severe liver injury, a higher probability of liver cirrhosis and a higher incidence of hepatocellular carcinoma. Treatment of these patients represents a therapeutic challenge. We report the case of an hepatitis B virus-hepatitis C virus co-infected patient, which particularly illustrates the interactions between these two viruses and therapeutic problems caused by the dual infection. HCV was initially dominant, which indicated a combination therapy by pegylated interferon and ribavirin. This treatment was associated with an early virological response of the HCV but an increase of HBV DNA occurred, requiring the use of a nucleoside analogue. A good response was obtained for the HBV but a relapse of HCV was noted, posing a problem for therapeutic decision. Copyright © 2012 Elsevier Masson SAS.

PMID: 22959099



Coinfection with hepatitis B and hepatitis C viruses can occur because of shared routes of infection. Coinfected patients have different viral replication, immunological profile and clinical course compared to monoinfected patients by hepatitis B virus (HBV) or hepatitis C virus (HCV). They have a more liver disease and an increased risk of hepatocellular carcinoma.

Our case illustrates the interactions between the viruses and therapeutic problems. HCV (genotype 1b) was the dominant virus in the 40 year-old patient (Metavir score A3F4). HBV DNA rate was < 2000 IU/mL. A pegylated bitherapy was prescribed and an early virological response was obtained for the HCV (undetectable RNA at week 12). As the HBV wasn’t inhibited by the HCV, its DNA rate increased at week 24 (7686 IU/mL), indicating a nucleoside analogue (Entecavir). At week 48 of pegylated bitherapy (corresponding to week 12 of treatment by entecavir), both HCV RNA and HBV DNA were undetectable. A relapse for the HCV occurred (HCV RNA 859242 IU/mL 24 weeks after the end of pegylated bitherapy) while the HBV DNA remained undetectable. We discussed using a triple therapy in association to the nucleoside analogue but to date no studies have documented the results of this strategy.

The HCV infection can suppress HBV replication, decreasing activity of HBV DNA polymerase, expression of HBsAg and hepatitis B core antigen in the liver compared to mono-infected persons. Furthermore, patients with chronic HBV infection who are superinfected with HCV can undergo seroconversion of HBeAg and HBsAg. The HBV can also suppress HCV replication and the two viruses could alternate their dominance during the different periods of co-infection, during and after treatment.

If the HCV is dominant, treatment with pegylated bitherapy is recommended as in monoinfection. Results of treatment are the same and sometimes better than in groups of monoinfected persons. If reactivation of HBV occurs during or after HCV clearance, HBV nucleotide/nucleoside is indicated.


 Figure 1: Hepatitis B virus

fig2Figure 2: Hepatitis C virus


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Dr Lamine Hamzaoui

Mohamed Tahar Maamouri Hospital – Nabeul – Tunisia

Department of gastroenterology

Gastroenterologist – Senior registrar

Faculty of medicine of Tunis – Tunisia


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