title: Hepatitis C viral genotype influences the clinical outcome of patients with acute posttransfusion hepatitis C.
abstract: Most patients with an acute infection of hepatitis C virus (HCV) will develop chronic hepatitis, and only about 15-20% of the cases will resolve spontaneously. The mechanism for the different outcomes in patients with acute HCV infection remains unclear. HCV genotype has been recognized as an important factor affecting the clinical course and outcome of chronic hepatitis C patients. In order to evaluate the role of HCV genotype in the clinical course and outcome of acute posttransfusion hepatitis C, 67 patients with acute posttransfusion hepatitis C from a prospective study of posttransfusion non-A, non-B hepatitis were enrolled. Thirty-nine patients (58.2%) were HCV genotype 1b. Among the 67 patients with acute posttransfusion hepatitis C, 53 (79.1%) progressed to chronic hepatitis. Significantly more patients with genotype 1b than non-1b genotypes developed chronic hepatitis (89.7% vs. 64.3%; P = 0.019). There was no significant difference in gender, mean age, amount of transfused blood, hepatitis symptoms, jaundice, incubation period, peak serum alanine transaminase, or serum HCV RNA titer between patients with HCV genotype 1b and non-1b infections. Patients who developed chronic hepatitis had a significantly greater incidence of genotype 1b infection (66.0% vs. 28.6%; P = 0.013) and a longer incubation period (7.3 weeks vs. 5.4 weeks; P = 0.052) than patients whose infection was resolved. Patients with a genotype 1b infection that resolved itself spontaneously all had an incubation period of less than 6 weeks. Multivariate logistic regression analysis revealed that genotype 1b and an incubation period > or = 6 weeks were significant predictive factors for the development of chronic hepatitis. Therefore, the HCV genotype can influence the outcome of patients with acute HCV infection.
authors.affiliation: Department of Family Medicine, Veterans General Hospital-Taipei, National Yang-Ming University School of Medicine, 201 Shih-Pai Road, Section 2, Taipei, 11217, Taiwan, Republic of China.
authors.forename: S J
authors.initials: SJ
authors.lastname: Hwang
authors.forename: S D
authors.initials: SD
authors.lastname: Lee
authors.forename: R H
authors.initials: RH
authors.lastname: Lu
authors.forename: C W
authors.initials: CW
authors.lastname: Chu
authors.forename: J C
authors.initials: JC
authors.lastname: Wu
authors.forename: S T
authors.initials: ST
authors.lastname: Lai
authors.forename: F Y
authors.initials: FY
authors.lastname: Chang
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D004279:DNA, Viral / Q000032:analysis; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000145:classification / Q000235:genetics* / Q000472:pathogenicity; D006526:Hepatitis C / Q000503:physiopathology* / Q000635:transmission / Q000821:virology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D020133:Reverse Transcriptase Polymerase Chain Reaction; D065227:Transfusion Reaction
chemical_list: D004279:DNA, Viral; D012367:RNA, Viral