Human hepatitis G virus (HGV) antibody (IgG)ELISA kit

Following the development of tests for hepatitis C virus and hepatitis E virus infection, it became clear that there remained cases of hepatitis that were non-A-E. Such cases provided impetus for the search for additional hepatitis viruses and, by using molecular techniques, several candidates were identified. An enteric agent responsible for sporadic non-A and non-E hepatitis was tentatively called hepatitis F virus. However, the lack of any corroborating reports has cast doubt on its status as a true hepatitis virus. Two groups independently reported the isolation of a blood-borne virus, designated as hepatitis G virus (HGV) and GB virus C (GBV-C) by their respective discoverers. They were later shown to be isolates of the same virus. While the virus has a high prevalence in cases of non-A-E hepatitis, it also has a high prevalence in the appropriate control groups and convincing evidence for its replication in the liver is lacking. Another possible hepatitis virus, TT virus, was discovered in the blood of a patient with post-transfusion non-A-E hepatitis. By using PCR primers designed to overcome the high nucleotide sequence divergence, TT virus was found to be ubiquitous with a worldwide distribution. A disease association is thus unlikely. Most recently, a DNA virus designated as SEN-V has been announced as a major cause of non-A-E hepatitis. Based on limited data available to researchers, SEN-V is the most convincing contender for the new hepatitis virus title. However, the lessons learnt from the hepatitis virus pretenders will need to be applied to SEN-V and any future contenders.

Several studies have shown that individuals co-infected with GB virus type C (GBV-C), and human immunodeficiency virus (HIV) have slower progression to acquired immunodeficiency syndrome (AIDS) and a prolonged lifespan, compared to those infected with only HIV. In Singapore, despite the steadily increasing number of HIV infections in recent years, there are no studies documenting the extent of GBV-C/HIV co-infection in this group of patients. To fill this dearth of information, two GBV-C screening assays was performed on 80 archived HIV-1-positive samples from the National University Hospital. The overall prevalence of GBV-C co-infection among patients infected with HIV in this study was 10% (8/80). Phylogenetic analysis of the eight dual-infection cases revealed that genotypes 3 (4/8, 50%) and 2a (2/8, 25%) were the main genotypes circulating among these Singaporean HIV patients. One case each of genotypes 2b (1/8, 12.5%) and 4 (1/8, 12.5%), which have not been described previously in Singapore, were identified. These findings hint at the complex epidemiology of GBV-C in different patient groups and a larger study would be needed to characterize, and understand the potential clinical impact of GBV-C co-infection on the patients. J. Med. Virol. 86:737-744, 2014. (c) 2014 Wiley Periodicals, Inc.