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The binding of polyalbumin to hepatitis B virus (HBV)-associated envelope epitopes has been studied by means of a radioimmunoprecipitation technique. HBV particles were purified from the sera of chronic hepatitis B surface antigen (HBsAg) carriers and labelled through the endogenous HBV-DNA polymerase reaction. Human albumin, polymerized through glutaraldehyde cross-linking, was able to precipitate (100 %) labelled HBV at concentrations of 31.2 and 62.5 μg/ml, in contrast to monomeric albumin (HSA). This event was further confirmed by immune electron microscopy. The addition of anti-HSA to the mixture HBV plus polyalbumin gave a 100% precipitation in a wide dilution range (15.6–500 μg/ml). The binding of polyalbumin (31.2 μg/ml) to virions was strongly inhibited (up to 98%) when preincubating with antibody to a glycosylation-dependent preS2 epitope on HBV. The same was accounted (up to 99%) for polyvalent IgG anti-HBs. However, antibodies to the group ‘a’ and subtype ‘d’ determinants, as well as anti-preS 1 region antibodies, inhibited weakly polyalbumin binding to HBV. The binding site of the inhibitor) antibody overlaps probably with neutralizing epitopes. Our findings support the hypothesi: that albumin binding plays an important role in the viral life cycle.

The correlation between the presence of liver membrane antibodies (LMA) and delta superinfection in chronic hepatitis B was studied in 136 chronic hepatitis patients, 20 hepatitis B surface antigen asymptomatic carriers and 50 healthy controls, by testing for the presence of LMA, hepatitis B virus markers and anti-delta (anti-HD). Neither anti-HD nor LMA were detected in controls or in asymptomatic carriers. LMA positivity was statistically higher (p < 0.001) in anti-HD-positive patients than in those with no anti-HD. Gamma globulin and glutamic pyruvic transaminase values were increased both in anti-HD- and LMA-positive patients with respect to those who were negative. In conclusion, a close association between the positivity to anti-HD and the presence of circulating LMA was found.

In order to determine the relationship between the presence of pre‐S1 and pre‐S2 proteins and the level of hepatitis B virus (HBV) replication, a study of 94 HBsAg chronic carriers, 15 anti‐HBe positive patients who suffered a viral reactivation and 12 HBeAg, HBV‐DNA positive cases under antiviral therapy, has been carried out. Pre‐S1 and pre‐S2 antigens were detected by RIA using polystyrene beads coated with anti‐preS1 or anti‐preS2 (Dr W. Gerlich, Göttingen) and 125I‐anti‐HBs as tracer. The presence of pre‐S1 and pre‐S2 antigens was detected in 74 (79%) and 85 (90%), respectively, out of the 94 HBsAg chronic carriers included. The level of these antigens was significantly higher in HBeAg, HBV‐DNA positive patients than in the other patients (p<0.05). Among anti‐HBe positive patients suffering a reactivation, a significant increase of pre‐S1 and pre‐S2 levels was observed, concurring with ALT exacerbation and HBV‐DNA positivity. After reactivation, the level of pre‐S antigens returned to the basal values. A significant decrease in pre‐S antigen levels (p<0.05) among patients who respond to recombinant interferon therapy was observed, while no changes were detected among non‐responder cases. The detection of pre‐S1 and pre‐S2 antigens in serum is more frequent in those patients with high viral replication. Furthermore, among anti‐HBe carriers with a viral reactivation, synthesis of pre‐S antigens takes place again.