Genetic Diversity and Molecular evolution of Hepatitis C Virus

Hepatitis C virus (HCV), an enveloped positive stranded RNA virus, is the causative agent of non-A, non-B (NANB) hepatitis (27). The virus was identified and characterized by molecular cloning techniques using serum from a NANB hepatitis virus infected chimpanzee (15) and based on the similarity of the genome organization and hydropathy profiles of several precursor proteins classified as a member of the Flaviviridae family. However, the low sequence homology compared to other flaviviruses eventually lead to its classification into a new genus hepacivirus, distinct from the other flavivirus members (33, 74). Initial studies demonstrated that blood transfusions were the main transmission route that caused the HCV epidemic, especially prior to the period of HCV-contaminated blood screening in 1992 (50). HCV high-risk groups include recipients of multiple blood transfusion, hemophiliacs, hemodialysis patients and intravenous drug users. Modes of transmission include contact with contaminated-blood products, sharing needles, mother-to-child and sexual transmissions (69). Infection of the human liver is often clinically benign, with mild symptoms in the acute phase and fulminant hepatitis is very rare. The disease may even go unnoticed in cases of acute resolving HCV. In most cases (>70%) HCV infection leads to chronic persistent or active infection, often accompanied by complications of liver cirrhosis, or type II cryoglobulinaemia. The mechanisms of

Molecular epidemiology of gibbon hepatitis B virus transmission

Although transmission of human hepatitis B virus (HBV) variants to nonhuman primates is well documented, it remains to be elucidated whether nonhuman primate HBV is transmissible to humans. The prevalence and transmission routes of gibbon HBV were analysed in 101 captive gibbons in Thailand. Approximately 40 % of these animals showed at least one marker of HBV infection; 19 animals were chronic HBV carriers, characterized by elevated levels of alanine amino transferase and the presence of HBV DNA. Some of the chronic animals were found to be anti-HBc (HBV core antigen) negative (4 of 19), while precore promoter point mutations (nt 1762 or 1764) were determined in four animals by RFLP analysis. Phylogenetic tree analysis of the complete surface gene sequences revealed that gibbon viruses clustered separately from hepadnaviruses of other hosts. Evidence for horizontal and vertical transmission in captive gibbons was obtained. HBV DNA was also detected in the saliva of HBV carrier gibbons. Although some of the animal caretakers at the Krabok Koo Wildlife Breeding Centre were found to be chronic HBV carriers, genotype and sequence analysis did not reveal any evidence for zoonotic disease transmission