Characteristics of dual infection of hepatitis B and C viruses among patients with chronic liver disease: a study from tertiary care hospital.

The major causes of chronic liver disease (CLD) are infection with Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) either alone or together. The clinical course of the disease varies in cases ofcoinfection with HCV and HBV as compared to single infection. The present study was carried out to determine the occurrence of coinfection of HCV with HBV in CLD patients and to look for the presence of suppressive effect of the two viruses on each other. The severity of liver disease was also assessed and correlated with biochemical profiles. Sera from 150 patients of CLD were tested serologically for the presence of HBsAg, IgG anti HBc and anti-HCV antibodies. HBV DNA and HCV RNA were also detected by amplifying surface region and 5' noncoding-core region respectively by polymerase chain reaction. Forty-seven (31.3%) cases showed the presence of HBsAg or anti IgG-HBc or HBV DNA either alone or together (Group A). Thirty-nine (26%) cases were found to be positive for HCV by detecting either anti-HCV antibodies or HCV RNA (Group B). Coinfection ofHCV with HBV (Group C) could be detected in twenty-four (16%) cases, of these twenty-one cases (87.5%) were positive both for HCV RNA and IgG anti-HBc without the presence of HBV DNA whereas in none of the cases could HBV DNA be detected in the absence of HCV RNA. Forty (26.6%) cases had neither HCV or HBV related CLD. Amongst, the biochemical parameters, the liver function test profiles were altered and found to be statistically significantly in HCV positive cases (Group B) when compared to the negative ones while in case of HBV (Group A) and coinfected (Group C) cases none of the parameters was statistically significant when compared with non-HBV and non-coinfected cases respectively. Thus, coinfection of HCV with HBV is seen in a substantial number of CLD cases. It is also revealed from the present study that HCV infection has a suppressive effect on the replication of HBV as seen by the loss of replicative markers like HBV DNA.