Analysis of Virus Genome in Sera from Patients with Silent Hepatitis B and Establishment of Detection Method for Antibodies against Virus

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We studied 10 patients with acute hepatitis, including 2 cases of fulminant hepatitis, that was not drug-induced, alcoholic, or autoimmune and in which viral markers for hepatitis A-E were negative. Hepatitis G virus genome was not amplified in sera obtained from the 10 patients with RT-PCR at 5'-untranslted and helicase regions. Hepatits B virus (HBV) genome was amplified in 8 of the 10 patients, including 2 cases of fulminant hepatitis, with nested PCR at the precore region. Futhermore, we studied other 5 patients with fulminant hepatitis, in which viral markers for hepatitis A-E were negative. HBV genome was also amplified in 4 of the 5 patients with nested PCR at the same region. Amplified PCR products were analysed with the direct sequencing method. The point mutation that changes codon 28 (TGG) of the precore region to stop codon (TAG) was recognized in 4 of the 6 patiedts with fulminant hepatitis. Although HBV genome was not amplified with nested PCR at the X region in all patients,but amplified at the preS2 region in 3 of 6 patients with fulminant hepatitis. By using the precore and preS2 regions as a foothold, we tried to analyse the sequence of residual unknown region with the primer walking method. However, we cannot get the useful results so far to establish the detecction method for antibodies against the silent HBV.