Interleukin-1 and interleukin-2 activity in chronic hepatitis B virus infection.

Abnormalities of lymphocyte proliferation in chronic hepatitis B virus infection are well documented, although the underlying mechanisms are poorly understood. To determine whether these defects may be secondary to disordered lymphokine production, we have simultaneously assayed interleukin-1 and interleukin-2 production in 31 chronic carriers of the hepatitis B virus. Supernatants from mononuclear cells cultured both in the presence and absence of lipopolysaccharide contained significantly increased quantities of interleukin-1 activity in patients compared with normal controls (p less than 0.

Expression of pre-S gene-encoded proteins in liver and serum during chronic hepatitis B virus infection in comparison to other markers of active virus replication.

Pre-S gene-encoded proteins of the hepatitis B virus (HBV) were studied in the liver by immunofluorescence and in serum by radioimmunoassay in 30 patients with chronic HBV infection. The results were compared with molecular hybridization analysis of HBV-DNA in liver and serum, with serum hepatitis B e antigen/antibody (HBeAg/anti-HBe) status and with underlying liver histology. Pre-S peptides were detected in the serum of 11 patients, 10 of whom were positive for serum HBV-DNA and/or liver hepatitis B core antigen.

Leucocyte hepatitis B virus DNA in acute and chronic hepatitis B virus infection.

In the present study we have investigated 53 patients with a spectrum of acute and chronic hepatitis B virus (HBV) infection for the presence of leucocyte HBV-DNA with the aid of molecular techniques. HBV-DNA was detected in peripheral blood mononuclear cells of 31 of 45 (69%) of chronic HBsAg carriers and 2 of 8 (25%) patients with acute hepatitis B. Although HBV-DNA was detected more frequently in leucocytes from those HBsAg carriers seropositive for HBeAg (79%), 50% of those with anti-HBe in serum had leucocytes positive for HBV-DNA independent of the presence of serum HBV-DNA.

Failure of exogenous interleukin 1 and interleukin 2 to correct decreased lymphocyte transformation in chronic hepatitis B virus carriers.

To test the hypothesis that reduced lymphocyte transformation in response to PHA in chronic hepatitis B virus infection might be due to deficient lymphokine production, lymphocyte transformation was measured in the presence or absence of exogenous interleukin 1, interleukin 2 or both, or, as a source of mixed lymphokines, supernatants from mixed lymphocyte reactions. The response to PHA was significantly impaired in patients compared to controls, but was not corrected by interleukin 1, interleukin 2 or supernatant from mixed lymphocyte reactions over a wide range of concentrations. Variation of the proportion of monocytes in culture or the addition of indomethacin had no effect on lymphocyte transformation.