Two distinct types of hepatitis B virus core promoter variants

liver411

Two distinct types of hepatitis B virus core promoter variants in Yemeni
blood donors.

Sallam TA, Tong CY
Department of Microbiology, Faculty of Medicine and Health Sciences, Sana'a University, Sana'a, Republic of Yemen.

[Medline record in process]


Genetic variations in the basic core promoter (BCP) region of hepatitis B
virus (HBV) occur during the natural history of chronic HBV infection. This
study investigates the presence of basic core promoter variations in 28
asymptomatic Yemeni blood donors, correlating variations with HBeAg
phenotype and viral load. The core promoter/precore and surface gene region of HBV DNA were amplified using nested PCRs and the PCR products were sequenced either directly or after cloning. HBeAg and viral load were
measured when HBV DNA was detectable. Sequencing of 18 surface PCR products indicated that all were of genotype D. Two distinct types of variants were
identified in the basic core promoter: substitution only (N = 14) and major
deletion (N = 9). The commonest substitutions were located at nucleotide
positions 1753, 1762, and 1764; 10/14 (71.4%) were associated with the
precore 1896A substitution resulting in the premature stop of the precore
reading frame and 6/14 (42.9%) had viral loads above 400 copies/ml. Two
forms of deletion variants were found: 8 bp deletion (1763-1770) (N = 2) and a novel 12 (1746-1757) + 8 bp (1763-1770) deletion (N = 7). The deletion sequences were never associated with the precore 1896A substitution and all had viral load below 400 copies/ml with negative HBeAg phenotype. The polymorphism 1773C was found in 9/14 (64.3%) substitution sequences whereas all deletion sequences had 1773T. Two donors had mixed sequences of basic core promoter substitution and major deletions (both 8 bp and 12 + 8 bp). While the deletion variants in these two donors were similar to others found in isolation, the substitutions were of a different pattern. Further studies are required to understand the selection process behind these variants. J.
Med. Virol. 68:328-334, 2002. Copyright 2002 Wiley-Liss, Inc.

PMID: 12226818, UI: 22213616