Virologic and Clinical Expressions of Reciprocal Inhibitory Effect of Hepatitis B, C, and Delta Viruses in Patients With Chronic Hepatitis

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Abstract
We studied 648 hepatitis B surface antigen (HBsAg)– and/or anti-hepatitis C virus (HCV)–positive patients to evaluate the virologic and clinical characteristics of multiple hepatitis viral infection. We defined as Case B–C an HBsAg/anti–HCV positive patient and as Case b–C an anti–HCV/anti–HBc–positive, HBsAg/anti–HBs-negative patient. For each Case B–C we scheduled as Control–B an HBsAg positive and anti–HCV negative patient and as Control–C an HBsAg/anti–HBs/anti-hepatitis B core antigen (HBc)–negative and anti–HCV-positive patient. Control group C was used as the control also for Case group b–C. Serum HBV DNA by molecular hybridization was found more frequently in Control group B (54% of 161 patients) than in Case group B–C (35.7% of 84, P < .01). The prevalence of HBV wild type was similar in Case group B–C (14.3%) and in Control group B (17.4%), whereas the e–minus strain was less frequent in Case group B–C (10.7% vs. 33%; P < .01). HBV DNA by polymerase chain reaction (PCR) was detected in 40.8% of 71 patients in Case group b–C. HCV RNA was detected more frequently in Control group C (90.7% of 130 patients) than in Case group B–C (65.2% of 69, P < .0001). Moderate or severe chronic hepatitis or cirrhosis were more frequent in Case group B–C (62.9% of 65 patients) than in Control group B (46.7% of 90, P < .05) or C (40.8% of 98, P < .005), and in Case group b–C (71.1% of 76) than in Control group C. Thus, in multiple hepatitis we observed a reciprocal inhibition of the viral genomes and a more severe liver disease. In Case group b–C, serum HBV DNA was frequent and the clinical presentation was severe.