A case-control study for clinical and molecular biological differences between hepatitis B viruses of genotypes B and C

Citation
E. Orito et al., A case-control study for clinical and molecular biological differences between hepatitis B viruses of genotypes B and C, HEPATOLOGY, 33(1), 2001, pp. 218-223
Citations number
40
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
HEPATOLOGY
ISSN journal
02709139 → ACNP
Volume
33
Issue
1
Year of publication
2001
Pages
218 - 223
Database
ISI
SICI code
0270-9139(200101)33:1<218:ACSFCA>2.0.ZU;2-X
Abstract
Clinical and molecular virological differences were evaluated in 50 Japanes e patients chronically infected with HBV of genotype B and C who were match ed for age and sex as well as the severity of liver disease in a case-contr ol study. Hepatitis B e antigen (HBeAg) was significantly less frequent (16 % vs. 42%, P < .01), whereas antibody to HBeAg (anti-HBe) was significantly more common (84% vs. 56%, P < .01) in genotype B than C patients. The pred ominance of mutants with G-to-A mutation at nucleotide (nt) 1896 in the pre core region (A1896) over the wild-type was comparable between genotype B an d C patients (60% and 62%, respectively), and it correlated with anti-HBe. The double mutation in the basic core promoter (A-to-T at nt 1762 and G-to- A at nt 1764), however, was significantly more frequent in genotype C than B patients (58% vs. 16%, P < .01), and it did not correlate with anti-HBe o r HBeAg, By the multiple logistic regression analysis, the double mutation in the basic core promoter (T1762/A1764) was significantly associated with genotype C [odds ratio (OR), 9.3; 95% confidence interval(CI), 3.4-25.1], a ge <greater than or equal to> 35 years (OR, 5.5; CI, 1.5-20.5), and more ad vanced liver disease (OR, 4.1; CI, 1.6-10.2), but it was not associated wit h sex, HBeAg, HBV DNA, or the precore mutation (A1896). These results sugge st a role of the double mutation in the basic core promoter in association with genotype C and a longer duration of infection in the aggravation of ch ronic hepatitis B.