In uitro synthesis of the anti-HBc, anti-HBs and polyclonal IgG and IgM classes of antibodies were determined from supernatants of peripheral blood mononuclear cells cultured in the presence of pokeweed mitogen. Thirty-seven patients with chronic hepatitis B and 10 healthy control subjects whose sera were positive for anti-HBs formed the study group. Twenty-four of 37 patients showed histologic evidence of chronic active hepatitis B while the remaining 13 patients had chronic persistent hepatitis B. Lymphocytes from chronic persistent hepatitis B, chronic active hepatitis B and healthy controls secreted similar levels of IgM. However, IgG synthesis was markedly impaired (p < 0.002) in the chronic persistent hepatitis B group as compared with healthy controls or chronic active hepatitis B patients. In uitro anti-HBc production and serum anti-HBc titers correlated directly with hepatocellular inflammation and inversely with serum hepatitis B virus DNA. Anti-HBc synthesis was significantly higher in chronic active hepatitis B patients who exhibited a more pronounced hepatocellular damage when compared to chronic persistent hepatitis B patients who had little or no liver cell injury.
Following infection by hepatitis B virus (HBV), the majority of patients recover, clear HBsAg and produce both anti-HBs and anti-HBc. However, after an acute infection, up to 10 to 15% of patients develop chronic hepatitis B. Their sera remain positive for HBsAg and anti-HBc, but remain negative for anti-HBs. Within this group of chronically infected patients, some will develop chronic active hepatitis B (CAH-B) with evidence of ongoing hepatocellular necrosis. The remainder will develop chronic persistent hepatitis, a relatively benign condition with minimal hepatic inflammation.
Nonspecific parameters of immune function, such as leukocyte migration inhibition and lymphocyte transformation techniques, have not demonstrated a generalized immune defect in patients with minimal hepatocellular damage (1-3). Numerous reports on lymphocyte phenotypes have shown that, during the acute phase of HBV infection, there is an increase in the numbers of Tcytotoxic/suppressor lymphocytes, but conflicting re-