HCV May Inhibit HBV Replication in HCV-HBV Coinfected Patients

Considered together, hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are the most prevalent causes of chronic liver disease globally. Due to overlapping routes of transmission, many individuals are coinfected with both viruses, but past research suggests that the 2 viruses may inhibit one another.

Hepatitis B is endemic in Taiwan, and most patients are infected early in life, often through mother-to-child transmission before or during birth. Clinical data from chronic HBV carriers superinfected with HCV in Taiwan suggest that active HCV infection may inhibit HBV replication. Taiwanese researchers sought to clarify this phenomenon in a study presented at both the annual meeting of the European Association for the Study of the Liver (EASL) last month in Milan and at the Digestive Disease Week (DDW) 2008 conference this week in San Diego.

The study examined a subset of participants in the REVEAL-HBV trial, which assessed the incidence of and risk factors for hepatocellular carcinoma (HCC) in individuals with hepatitis B. Only patients with complete hepatitis B surface antigen (HBsAg), anti-HCV antibody, and alanine aminotransferase (ALT) data from serum samples taken at study entry were included in these analyses.

HBV DNA and HCV RNA levels were measured in HBsAg positive and anti-HCV antibody positive patients, respectively. Among patients coinfected with both viruses, the relationship between HBV DNA and HCV RNA levels was evaluated first by correlation analyses and then using a multivariable linear regression model adjusting for age, sex, and serum ALT level.

Results

• Of the 23,820 subjects in the cohort, 23,785 had complete HBsAg and anti-HCV data.

• Of these, 3931 were infected with HBV alone, 1095 had HCV alone, and 218 were coinfected with HBV and HCV.

• The prevalence of anti-HCV antibody positivity was 5.6% for HBsAg positive and 5.3% for HBsAg negative individuals (P=0.41).

• HBV DNA was detectable in 76% of anti-HCV negative subjects compared with 60.5% of anti-HCV positive individuals (P<0.001).

• Mean HBV DNA levels were 3.62 vs 2.74 log copies/mL, respectively.

• HBV DNA and HCV RNA were tested in 181 of 218 coinfected patients; in this group, HBV and HCV viral loads were negatively correlated (R = -0.26; P<0.001).

• After adjusting for patient age, sex, and ALT levels in a multivariable linear regression analysis, serum HBV DNA levels increased as serum HCV RNA levels decreased (R = -0.24; P<0.001).

Conclusion

Based on their findings, the investigators concluded, "The results of this study suggest a likely interference in the replication levels of HBV and HCV rather than in the seroprevalence of HBsAg and anti-HCV."

In addition they wrote, "In an HBV-endemic area like Taiwan, where HBV infection usually occurs early while HCV infection occurs later in life, HBV replication may be negatively influenced by the replication of HCV."

5/20/08

References

CL Jen, HI Yang, CJ Liu, and others. Negative correlation between hepatitis B and hepatitis C viral load in co-infected persons. 43rd annual meeting of the European Association for the Study of the Liver (EASL 2008). Milan, Italy. April 23-27, 2008.

CL Jen, HI Yang, CJ Liu, and others. Negative correlation between hepatitis B (HBV) and C (HCV) viral load in co-infected persons. Digestive Disease Week (DDW) 2008. San Diego, CA. May 17-22, 2008. Abstract T1018.