E. Sagnelli et al., Virologic and clinical expressions of reciprocal inhibitory effect of hepatitis B, C, and delta viruses in patients with chronic hepatitis, HEPATOLOGY, 32(5), 2000, pp. 1106-1110
We studied 648 hepatitis B surface antigen (HBsAg)- and/or anti-hepatitis C
virus (HCV)-positive patients to evaluate the virologic and clinical chara
cteristics 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-C HBc-pos
itive, HBsAg/anti-HBs-negative patient. For each Case B-C we scheduled as C
ontrol-B an HBsAg positive and anti-HCV negative patient and as Control-C a
n HBs/anti-HBs/anti-hepatitis B core antigen (HBc)-negative and anti-HCV-po
sitive 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 (1
4.3%) and in Control group B (17.4%), whereas the e-minus strain was less f
requent in Case group B-C (10.7% vs. 33%; P < .01), HBV DNA by polymerase c
hain 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 pati
ents) than in Case group B-C (65.2% of 69, P < .0001). Moderate or severe c
hronic hepatitis or cirrhosis were more frequent in Case group B-C (62.9% o
f 65 patients) than in Control group B (46.7% of 90, P < .05) or C (40.8% o
f 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 v
iral genomes and a more severe liver disease. Tn Case group b-C, serum HBV
DNA was frequent and the clinical presentation was severe.