Viral Replication In Patients Research Articles

Persistence of Serum Hepatitis B Virus Deoxyribonucleic Acid in Hepatitis B Surface Antigen-Positive Patients With Chronic Persistent Hepatitis Treated With Predhisone

The effect of a short course of prednisone therapy was evaluated in 8 patients with liver biopsy-verified chronic persistent hepatitis B. In 6 of the 8 (75%) patients, an abrupt fall in serum alanine aminotransferase levels after the initiation of prednisone was noted, and in 4 patients, there was an increase in serum alanine aminotransferase values after prednisone was discontinued. However, the serum levels of hepatitis B virus deoxyribonucleic acid were consistently greater than or equal to 200 pg before, during, and after the course of treatment in 7 of the 8 (87.5%) patients. All patients were initially hepatitis B e antigen-positive and remained so during the study period. These findings indicate that, unlike some patients with chronic active hepatitis B, immunosuppression with prednisone had no effect in altering hepatitis B viral replication in patients with chronic persistent hepatitis.

Activities of 2'-5'oligoadenylate synthetase in peripheral blood mononuclear cells of patients with viral hepatitis, and chronic type B hepatitis during interferon therapy.

The activities of the interferon-induced enzyme 2'-5' oligoadenylate synthetase in peripheral blood mononuclear cells were determined in patients with viral hepatitis. Increased levels of the enzyme were found in patients with acute type B hepatitis at the early phase and also in those with chronic type B hepatitis at the active stage. The levels of this enzyme activity were not significantly increased in patients with acute type A hepatitis or in those with acute type non A non B hepatitis. However, in two patients with acute type A hepatitis the levels of this enzyme were elevated shortly at the onset. These results support the hypothesis that an endogenous interferon response in patients with acute type A hepatitis and in those with acute type B hepatitis may be instrumental in the modulation of these types of hepatitis virus infections. Whereas hepatitis non A non B virus replication in patients with acute type non A non B hepatitis may be associated with poor interferon response. The activities of the enzyme in peripheral blood mononuclear cells were determined in patients with chronic type B hepatitis during interferon therapy. Increased levels of the enzyme were found in all patients during interferon therapy. This increase correlated well with the decreased DNA-polymerase activities. The data also showed that assay of this enzyme activity is useful to determine the optimal dosage and means of interferon therapy for chronic type B hepatitis.

Liver disease activity and hepatitis B virus replication in chronic delta antigen-positive hepatitis B virus carriers.

Delta antigen is currently thought to reflect superinfection of the liver with a defective RNA virus (delta agent), requiring helper function from hepatitis B virus for its replication. To assess the influence of delta agent on hepatitis B virus replication in patients persistently infected with both viruses and showing chronic liver disease, we measured serum and liver hepatitis B virus DNA in HBsAg-positive chronic liver disease patients who were either positive or negative for delta antigen in the liver. Hepatitis B virus DNA was assayed in the serum of 21 patients with delta antigen-positive/HBsAg-positive chronic liver disease and in 21 patients with delta antigen-negative/HBsAg-positive chronic liver disease matched for HBeAg/anti-HBe status and underlying liver histology. HBcAg and delta antigen in liver was determined by immunofluorescence or immunoperoxidase staining. In delta antigen-positive/HBsAg-positive chronic liver disease, serum hepatitis B virus DNA was detected transiently in 4 of 21 cases (19%) and was present in these patients at low levels (trace to 2+). In contrast, 9 of 21 (43%) delta antigen-negative/HBsAg-positive chronic liver disease patients were serum hepatitis B virus DNA positive, and five of these had high serum hepatitis B virus DNA levels (3+ to 4+). Serum HBsAg and anti-HBc titers were significantly lower in delta antigen-positive cases and correlated with reduced amount of HBcAg in the liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Immunosuppressive Therapy on Viral Markers in Chronic Active Hepatitis B

Hepatitis B virus associated DNA polymerase activity, hepatitis b surface antigen (HBsAg), and serum aspartate aminotransferase were followed in 21 patients with chronic active hepatitis while immunosuppressive therapy (prednisone +/- azathioprine) was being withdrawn. In every case, DNA polymerase activity fell within 6-10 wk of decreasing treatment and became undetectable in 8 patients. This was usually accompanied by a fall in HbsAg titer and a transient rise in serum aspartate aminotransferase activity. Four additional patients with previously untreated HbsAg positive chronic active hepatitis were placed on prednisone for 12 wk. There was a rise in DNA polymerase activity and HBsAg titer with a fall in serum aspartate aminotransferase values during treatment. Upon discontinuing therapy, DNa polymerase activity fell dramatically in all 3 patients who completed their course of prednisone and became undetectable in 1. These findings suggest that immunosuppressive therapy has a potentiating effect on hepatitis B viral replication in patients with chronic active hepatitis.