Wednesday, January 25, 2012
hepatitis C virus
HISTORICAL BACKGROUND
The hepatitis C virus is a small, spherical enveloped RNA virus approximately 50 nm diameter. Its buoyant density in sucrose is only 1.06 g/cm3 but much of the virus in chronically infected individuals appears to be bound to antibody, which imparts a higher density of approximately 1.17g/cm17.
Genomic organization of hepatitis C virus shows A 5’ non-coding (NC) region consists of approximately 340 nucleotides and contains an apparent internal ribosomal entry site (IRES). Immediately downstream is a single large open reading frame (ORF) of approximately 9,000 nucleotides, encoding a large poly protein precursor of approximately 3,000 amino acids that is co-translationally or post-translationally cleaved into separate proteins by a combination of host and viral proteases. A capsid protein, two envelope proteins (E1 and E2), and a small protein (P 7) of unknown function are encoded in the 5’ region of the ORF.
At least six nonstructural proteins, including protease, helicase, and RNA polymerase enzymes and regulatory peptides, are arrayed in the 3’ portion of the ORF. Finally, there is a 3’ NC region that consists of approximately 50 nucleotides, a polypyrimidine tracked and a highly conserved terminal sequence of approximately 100 nucleotides. Testing for HCV infection typically involves analysis of a serum sample for anti-HCV antibody and for viral genomic DNA. However, current diagnostic tests are often limited in the sensitivity ith which they can detect genetically and serologically altered HCV strains.
The mechanism of liver injury in acute and chronic hepatitis C type is unknown, but since there is little evidence as to the cytopathogenicity of HCV, it is thought that liver damage may in fact be mediated by the host’s cellular immune response to the infection. Given the lack of definitive symptoms, liver histology and the circulating levels of liver enzymes are currently considered to be the most reliable predictors of progression to cirrhosis. Studies show that severe necro-inflammatory activity, as well as severe fibrosis in hepatic tissue, both due to elevated levels of liver enzymes can be correlated with progression to cirrhosis within 10 years. In cases where inflammation and fibrosis is mild, progression is slowed and even limited
Factors influencing the rate of progression of chronic hepatitis C to cirrhosis and liver cancer include alcohol abuse, the duration of the infection and possibly viral titer.
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Hepatitis c virus
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