Histopathology and localization of viral antigens in the liver of HB_sAg positive homosexuals

Abstract

In a survey of the prevalence of chronic hepatitis B in a male homosexual population, liver biopsies were done in 28 asymptomatic patients who had persistently raised aminotransferases. Four patients had active cirrhosis (AC), 13 had chronic active hepatitis (CAH) of various degrees of severity and 11 had either chronic persistent hepatitis (CPH) or minor changes of the type seen in hepatitis B virus carriers. Core associated antigens and surface antigen, were demonstrated by the PAP immunoperoxidase method in 20 cases. Core and surface antigens tended to be present in the same areas of the biopsy and quantitation showed higher core to surface antigen ratios in CAH than in CPH, the difference being statistically significant. In seven cases no core-associated antigens were demonstrated in the presence of surface antigen: most of these patients had either inactive disease or active cirrhosis. In one carrier neither antigen was demonstrated. Ten patients had two or more biopsies. Four of these had no treatment and the amounts of core and surface positive cells in the liver did not increase. Six were treated with immunosuppressants. This did not alter the degree of either inflammation or fibrosis. but the number of surface and core antigen positive cells in the liver was higher after treatment in almost every case.

Hepatitis A Virus and Non-A, Non-B Virus Superinfections in HBsAg Chronic Carriers

“…Our data suggest that the superinfections do not cause more severe disease and do not influence the clinical course of the HBsAg chronic carriers. Our observations indicate that a careful diagnosis of hepatocytolysis is necessary in HBV chronic infection, in order to discriminate causes that are able to induce severe damage in underlying disease.Carrying HBV is a lifelong condition; however, HBsAg is cleared by 1-2% of the HBV-infected patients each year [1].Many factors modify the natural history of HBV chronic infection: serum conversion of HBeAg to anti-HBe [2,3], the delta agent (HDV) -an incomplete RNA virus which only replicates in the presence of HBV [4-6], immunosuppressive drugs that are capable of inducing viral replication [7][8][9][10][11], and al cohol intake which may accelerate the pro cess of liver deterioration and/or the devel opment of cancer in chronic HBsAg carriers [12,13]. The presence of HBV infection does not induce cross-immunity, hence it does not afford protection against HAV and non-A, non-B hepatitis [14,15].…”