AIM: To investigate the state of infection, replication site,pathogenicity and clinical significance of transfusiontransmitted virus (TTV) in patients with hepatitis, especiallyin patients of unknown etiology.METHODS: Liver tissues taken from 136 cases of non-A non-G hepatitis were tested for Tr virus antigen and nucleic acidby in situ hybridization (ISH) and nested-polymerase chainreaction (PCR). Among them, TT virus genome and itscomplemental strand were also detected in 24 cases ofautopsy liver and extrahepatic tissues with ISH. Meanwhile,TTV DNA was detected in the sera of 187 hepatitis patientsby nested-PCR. The pathological and clinical data of thecases infected with nv only were analyzed.RESULTS: In liver, the total positive rate of rrv DNA was32.4 % and the positive signals were located in the nuclei ofhepatocytes. In serus, rrv DNA was detected in 21. 4 %cases of hepatitis A-G, 34.4 % of non-A non-G hepatitis and15 % of healthy donors. The correspondence rate of lrvDNA detection between liver tissue with ISH and sera withPCR was 63.2 % and 89.3 % in the same liver tissues by ISHand by PCR, respectively. Using double-strand probes andsingle-strand probes designed to detect TTV genome, thecorrespondence rate of Trv DNA detected in liver andextrahepatic tissues was 85. 7 %. Using single-strandprobes, TTV genome could he detected in liver andextrahepatic tissues by PCR, but its complemental strands(replication strands) could be observed only in livers. Theliver function of most cases infected with TTV alone wasabnormal and the liver tissues had different pathologicaldamage such es ballooning, acidophilia degeneration,formation of apoptosis bodies and focus of necrosis, but the inflammation in the Iobule and portal area was mild.CONCLUSION: The positive rate of TTV DNA among cases ofhepatitis was higher than that of donors, especially inpatients with nonA non-G hepatitis, but most of them werecoinfected with other hepatitis viruses. Lrv can infect notonly hepatocytes, but also extrahepstic tissues. However,the chief replication place may be liver. The infection of lrvmay have some pathogenicity. Although the pathogenicity iscomparatively weak, it can still damage the liver tissues.The lesions in acute hepatitis (AH) and chronic hepatitis(CH) am mild, but in severe hepatitis (SH) , it can be veryserious and cause liver function failure, therefore, we shouldpay more attention to TTV when studying the possiblepathogens of so-called "liver hepatitis of unknown etiology".