V. Hepatitis G HG

V. Hepatitis G (HG)

In 1969, German researchers Dinhad et al. injected serum from a hepatitis A patient into cynomolgus monkeys, inducing the formation of a novel viral particle that was neither hepatitis A nor hepatitis B nor hepatitis C. This particle was subsequently successfully passaged repeatedly. In 1995, British physician Karayialznk detected particles in the serum of the same cynomolgus monkeys and conducted a series of studies on these particles. His research confirmed that these particles possessed significant pathogenic properties and was certified by international medical experts as HGV, with the disease they caused being named HG. HGV is a positive-strand RNA virus with a diameter of less than 100 nanometers. The prevalence of HGV in China ranges from 8% to 16.7%, while statistics from four counties in the United States show a prevalence of 9%, and West Africa sees a prevalence of 19.9%. Transmission of this disease is primarily through bloodborne routes, including blood transfusions, blood products, hemodialysis, intravenous drug use, mother-to-child transmission, and organ transplantation. HG is also known as cytomegalic hepatitis, commonly affecting children, though it occasionally occurs in adults. Due to its mild clinical symptoms—almost no symptoms are noticeable—the disease is often asymptomatic, yet 59% of patients exhibit elevated ALT levels. Among those with elevated ALT, nearly 79% also have other hepatitis infections. HG alone rarely causes jaundice or hepatomegaly. For this reason, some people still question the pathogenicity of HGV.