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Abstract
Hepatitis G virus is a single-stranded, positive sense RNA virus, belonging to the family Flaviviridae. It is a hepatotrophic virus discovered in 1995. HGV also replicates in PBMCs as T and B lymphocytes. It is highly prevalent among volunteer blood donors and general population, as many cases can be chronic carriers for HGV for decays with no symptoms. Although HGV infection alone rarely causes acute hepatitis with transient elevation of ALT and AST, about 10-20% of infections develop chronic hepatitis with elevated serum ALT levels. HGV RNA was detected in patients with FHF of unknown etiology, and clinically characterized by sub-acute progression, continuing fluctuation of serum amino transferases, and high mortality. HGV also causes extra hepatic manifestations as hepatitis/ aplastic anaemia syndrome, preceeding hepatitis, and subsequent marrow failure. HGV co-infection with other hepatitis viruses as HCV, and HBV will worsen the case of chronic hepatitis leading to more progression and faster hepatic damage and increases the HCC incidence.
HGV is transmitted via exposure to blood and blood products; so infection is frequent among multiple transfused haemophiliacs, thalassaemia and haemodialysis patients. Other routes of transmission such as sexual, vertical transmission, nosocomial, and intra-familial transmission have been documented.