HCV genetics and genotypes dictate future antiviral strategies

Louis Papageorgiou, Chrisanthy Vlachakis, Konstantina Dragoumani, Sofia Raftopoulou, Dimitrios Brouzas, Nicolas C Nicolaides, George P Chrousos, Evangelia Charmandari, Vasileios Megalooikonomou, Dimitrios Vlachakis

Abstract


At the end of the 1980s, the hepatitis C virus (HCV) was cloned and formally identified as the cause of the majority of non-A and non-B hepatitis cases. Today, around 170 million people worldwide are infected with HCV, making it five times more common than infection with the human immunodeficiency virus (HIV).  Several methods exist which mediate the spread of infection. One of the most common and efficient is sharing or re-using injecting equipment; studies have indicated that 80-90% of individuals in some populations of intravenous drug users test positive in serum HCV assays. Contracting HCV from infected blood transfusions was also a major cause of infection before screening tests were introduced in the early 1990s.  Other possible, but less common, methods of infection transmission include mother-to-child during pregnancy, sexual contact and nosocomial acquisition (for example between surgical or dialysis patients).  It appears that concurrent HIV-1 infection increases the risk of HCV transmission via the mother-to-child or sexual routes.


Keywords


HCV; Hepatitis C virus; hepatitis; Genetics; antiviral

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