[The effects of hepatitis E virus superinfection on patients with chronic hepatitis B: a clinico-pathological study].

OBJECTIVE

To observe the effect of hepatitis E virus (HEV) superinfection on hepatic lesion and hepatitis B virus (HBV) replication in patients with chronic hepatitis B (CHB).

METHODS

Totally 122 patients with CHB were enrolled in this study. They were tested for anti-HEV IgM and IgG in serum, amount of HBV DNA in serum and liver tissue obtained by liver biopsy and HBcAg expression in liver tissue. Other parameters such as ALT, total bilirubin (TBil), albumin (A) and globulin (G), gamma-electrophoretic protein (gamma-EP), prothrombin activity (PTA) were also measured. 21 of the 122 patients (17.2%) were found to have HEV superinfection and the remaining 101 were not. Repeat liver biopsy was performed after 1 year in 7 patients with HEV superinfection and 14 patients without. Moreover, HBV DNA amount in serum from 8 HBeAg negative patients with HEV superinfection were tested dynamically in acute and recovery stage of HEV infection.

RESULTS

Comparison of the data from the 21 patients with HEV superinfection and 101 without showed that there was no significant difference in the level of A/G ratio (1.74 +/- 0.50 vs. 1.83 +/- 0.37) and gamma-EP [(24.18 +/- 6.36)% vs. (22.27 +/- 4.59)%, P > 0.05]. However, the level of ALT [(244.61 +/- 81.07) U/L vs. (143.87 +/- 47.69) U/L] and TBil [(88.24 +/- 28.54) micro mol/L vs. (46.16 +/- 17.13) micro mol/L] was significantly higher (P < 0.05), but that of PTA lower in the group with HEV superinfection than in the group without superinfection [(58.57 +/- 17.44)% vs. (72.52 +/- 12.25)%, P < 0.05]. So were the amount of HBV DNA in serum [(5.45 +/- 1.86) copies/ml vs. (6.59 +/- 1.28) copies/ml, P < 0.05] and liver tissue [(6.96 +/- 2.52) copies/g vs. (8.47 +/- 1.79) copies/g, P < 0.05] as well as HBeAg and HBcAg positive rates (8/21 vs. 64/101; 9/21 vs. 67/101, P < 0.05). Pathologically, the hepatic inflammatory activity was more severer in patients with HEV superinfection, but the severity of fibrosis was not significantly different. There was no difference in the severity of inflammatory activity and stage of fibrosis between the 7 patients with HEV superinfection and the 14 patients without as well as before and after 1 year of treatment. The amount of HBV DNA and HBeAg positive rate in serum from recovery stage of HEV infection were higher than those of acute stage.

CONCLUSIONS

HEV superinfection leads to activation of hepatic pathological changes and worsens the inflammatory activity. Moreover, HEV superinfection inhibits HBV replication, but it may not be long-lasting.