title: Mechanisms involved in the development of chronic hepatitis C as potential targets of antiviral therapy.
abstract: At present, about 3% of the human population are infected with hepatitis C virus (HCV). The first, acute stage of the disease is usually asymptomatic. However, only 15-25% of the infected eliminate the virus, while the remaining patients develop chronic hepatitis C (CHC). After 10-30 years of CHC, cirrhosis occurs in 20-30% of patients; 5-10% of this group eventually suffer from hepatocellular carcinoma. Unfortunately, up till now no effective methods protecting against HCV or allowing for efficient CHC treatment have been elaborated. This is primarily because not much is known about the mechanism of CHC emergence and the factors affecting anti-HCV therapy. There are several lines of evidence that some specific features of the virus, especially its high genetic variability might be responsible for the maintenance of HCV infection. Moreover, a few mechanisms which affect host-virus interactions and can additionally support CHC development have recently been identified. Hybridization between the host-encoded, liver-specific microRNA (miR-122) and the 5'-untranslated region of HCV genome was shown to be required for effective viral RNA replication. It was also postulated that HCV proteins mimic some of the human ones; that is why the virus is not eliminated. Another hypothesis assumes that interactions between HCV E2 glycoprotein and CD81 receptor modulate various cellular pathways, thus supporting viral propagation. There is no doubt that a better understanding of the mechanisms described above is of great importance for designing new therapeutic strategies and anti-HCV drugs.
authors: Institute of Bioorganic Chemistry, Polish Academy of Sciences, Noskowskiego 12/14, 61-704 Poznan, Poland.
authors: Paulina
authors: P
authors: Jackowiak
authors: Magdalena
authors: M
authors: Figlerowicz
authors: Anna
authors: A
authors: Kurzyńska-Kokorniak
authors: Marek
authors: M
authors: Figlerowicz
mesh_terms: D000998:Antiviral Agents / Q000494:pharmacology* / Q000627:therapeutic use; D055808:Drug Discovery; D014644:Genetic Variation; D016174:Hepacivirus / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics / Q000378:metabolism; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000209:etiology / Q000821:virology; D054884:Host-Pathogen Interactions; D006801:Humans; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000821:virology; D035683:MicroRNAs / Q000378:metabolism; D012367:RNA, Viral / Q000378:metabolism; D060225:Tetraspanin 28 / Q000378:metabolism; D014759:Viral Envelope Proteins / Q000378:metabolism; D014779:Virus Replication / Q000187:drug effects
chemical_list: D000998:Antiviral Agents; C554798:CD81 protein, human; C531907:MIRN122 microRNA, human; D035683:MicroRNAs; D012367:RNA, Viral; D060225:Tetraspanin 28; D014759:Viral Envelope Proteins; C091015:glycoprotein E2, Hepatitis C virus