Clinicopathological features of serum TTV DNA-positive non-A-G liver diseases in Japan.

The clinical significance of GBV-C/HGV exposure in C-viral chronic liver disease and blood donors.



Background/Aims: This investigation compared the histological findings in the livers of chronic hepatitis C patients who were or were not co-infected with SEN virus (SEN-V) to determine the histological and clinical characteristics of SEN-V infection in Japan.



Methods: Three hundred and ninety-two patients with hepatitis C virus-associated chronic hepatitis (CH) or liver cirrhosis (LC) were included in the study. Serum samples were tested for the presence of SEN-V DNA by nested polymerase chain reaction. The liver biopsy specimen of each patient was examined and scores were assigned to indicate the severity of each of the following features: inflammatory cell infiltration in the periportal, parenchymal, and portal areas; F stage; portal sclerotic change; perivenular fibrosis; pericellular fibrosis; damage to the bile ducts; steatosis and irregular regeneration of hepatocytes (IR).



Results: Of the 473 patients, 194 (41.0%) were positive for SEN-V DNA. The rate of progression of F stage correlated with SEN-V DNA positivity. The blood biochemical parameters did not differ significantly between the SEN-V DNA-positive and -negative patients. The histological features of the livers of SEN-V DNA-positive patients included more severe parenchymal inflammatory cell infiltration and more IR. In particular, among those at the F2, F3 and F4 stages, the degree of IR of the SEN-V DNA-positive patients was significantly greater than that of the SEN-V DNA-negative patients. The cumulative probability of hepatocellular carcinoma (HCC) incidence and survival rate did not differ between the SEN-V DNA-positive and-negative patients.



Conclusions: SEN-V co-infection may influence the histopathological features of the livers of patients with type C CH and LC but does not affect the outcome of patients with type C chronic liver disease.

SEN virus infection influences the pathological findings in liver but does not affect the incidence of hepatocellular carcinoma in patients with chronic hepatitis C and liver cirrhosis.

The human pegivirus type 1 (HPgV-1)-as known as hepatitis G virus and GB virus C-is a common single-stranded RNA flavivirus. Because few studies have demonstrated an association between HPgV-1 infection and disease, screening for HPgV-1 is not performed routinely. Nonetheless, a beneficial impact of HPgV-1 infection on HIV disease progression has been reported in multiple studies. Given the burden of HIV in Asia and the complex interactions between viral co-infections and the host, we provide a comprehensive overview of the existing data from Asia on HPgV-1 infection, including the prevalence and circulating genotypes in all Asian countries with data reported. This review highlights the research conducted thus far and emphasizes the need for additional studies on HPgV-1 across the Asian continent.

Human pegivirus type 1 infection in Asia-A review of the literature.

Objectives: The aims of this study were to determine the hepatitis B virus (HBV) genotypes in hepatitis delta virus (HDV) RNA-positive patients and to characterize the HBV nucleotide sequences that may be found on a distant island of Japan. Methods: This study included three patients with chronic hepatitis who were positive for hepatitis B surface antigen (enzyme-linked immunosorbent assay; ELISA), HDV antibody (ELISA) and HDV RNA by polymerase chain reaction (PCR). The HBV genotype was determined by nested PCR using type-specific primers. The first-round PCR products from two patients were sequenced, followed by an investigation of nucleotide homology. Results: Viruses from all three patients in this study were classified as HBV genotype B. Comparison with HBV isolates from geographically neighboring regions revealed that the two HBV isolates had 97.9–98.6% identity at the nucleotide level to a Chinese isolate, 98.3–98.6% identity to the Okinawa isolate and 98.6–98.8% identity to a Japanese isolate of genotype B. On phylogenetic analysis, the HBV isolates from the two patients were classified as HBV genotype B. The HBV isolates of cases 1 and 3 clustered in the same group as isolates from the Chinese mainland and Japanese mainland, which are geographically near Miyako Island. Conclusion: The HBV isolates coinfected with HDV found on Miyako Island were of genotype B. The PCR method based on genotype-specific primers was useful in determining HBV genotypes.

Genotype Analysis, Using PCR with Type-Specific Primers, of Hepatitis B Virus Isolates from Patients Coinfected with Hepatitis Delta Virus Genotype II from Miyako Island, Japan

It is still unclear whether hepatitis G virus (HGV) and hepatitis C virus (HCV) co-infection influences the natural course of chronic HCV infection and the response to interferon (IFN) therapy. In this study, we investigated the HGV RNA changes and responses to IFN therapy of HGV RNA-positive hepatitis C patients. The presence of HGV RNA in 264 patients who received IFN therapy at our institute was examined using the nested reverse transcription-polymerase chain reaction with primers deduced from the 5' non-coding region (5'-NCR) of the HGV. We also analysed the nucleotide sequences of the 5'-NCR and HGV before and after IFN therapy. Twelve (4.5%) of the 264 patients with chronic hepatitis C were HGV RNA positive. Of these 12 patients, full information was available in nine. Of those nine, seven became HGV RNA negative during IFN therapy but in six of the seven a relapse occurred. HCV RNA was not detected 1 year after IFN therapy in six patients. The serum alanine aminotransferase (ALT) levels of all the HCV RNA-negative patients post-treatment was within the normal range, irrespective of their HGV RNA status. Nucleotide sequences did not change after IFN therapy in any patient. Hence, we confirm that HGV is sensitive to IFN therapy but the liver damage caused by HGV infection is very mild or does not modify the liver function tests.

Biochemical and virological response to interferon therapy in patients with chronic hepatitis C, co-infected with hepatitis G virus.

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Biochemical and virological response to interferon therapy in patients with chronic hepatitis C, co-infected with hepatitis G virus.