YEN-HSUAN NIMEI-HWEI CHANGLin K.-H.PEI-JER CHENDONG-TSAMN LINHONG-YUAN HSUDING-SHINN CHEN2021-07-032021-07-0319960031-3998https://www.scopus.com/inward/record.uri?eid=2-s2.0-84984538814&doi=10.1203%2f00006450-199602000-00022&partnerID=40&md5=3d56682eb7b1700951f2afb19db2fe93https://scholars.lib.ntu.edu.tw/handle/123456789/568859To determine and correlate the liver function profile, hepatitis C virus (HCV) genome, anti-HCV, genotypes, quantitation, and nucleotide sequence variability in polytransfused thalassemic children, 61 such children were studied prospectively for 4 y. Twenty-six had HCV infection. The average age, number of transfusions, and alanine aminotransferase (ALT) levels of the HCV- infected group were higher than those of the 35 children without HCV infection. None was infected after the initiation of anti-HCV screening in donor blood. Liver biopsies were performed in six HCV-infected and eight HCV- noninfected thalassemic children, and portal fibrosis was found more frequently in the HCV-infected group. Quantitation of HCV RNA was clone by the competitive polymerase chain reaction method, and the titer was about 1 x 106 to 5 x 108 copies/mL. The titer did not change significantly over the 4-y follow-up period and did not correlate with ALT levels. Nineteen HCV- infected patients were genotyped; 15 were Okamoto/Simmonds type II/1b, two were type III/2a, and two were type IV/2b. The hypervariable region of the HCV genome (E2/NS1) was cloned and sequenced in two serum samples from one patient collected at a 2-y interval, as the ALT levels decreased. The variation rate was estimated to be 1.2-1.7 x 10-2/nucleotide/y. The results showed that, in polytransfused thalassemic children, 43% (26/61) contracted HCV. We conclude that HCV infection may cause elevated ALT levels and portal fibrosis of the liver, whereas the viral titer and genotypes do not parallel ALT levels.[SDGs]SDG3alanine aminotransferase; hepatitis B surface antigen; adolescent; adult; article; controlled study; disease association; female; genetic variability; hepatitis C; human; human cell; liver biopsy; liver function test; major clinical study; male; priority journal; RNA analysis; thalassemiajournal article10.1203/00006450-199602000-0002288258072-s2.0-84984538814