Lack of association of RAD51 genetic variations with hepatitis B virus clearance and occurrence of hepatocellular carcinoma in a Korean population

✍ Scribed by Charisse Flerida A. Pasaje; Jeong-Hyun Kim; Byung-Lae Park; Hyun Sub Cheong; Joon Seol Bae; Tae-Joon Park; Jin-Sol Lee; Yongha Kim; Hyo-Suk Lee; InSong Koh; Yoon Jun Kim; Hyoung Doo Shin

• Publisher: John Wiley and Sons
• Year: 2011
• Tongue: English
• Weight: 203 KB
• Volume: 83
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.22122

✦ Synopsis

Abstract

The RecA homolog, E. coli (S. cerevisiae) (RAD51) may modulate hepatitis B virus (HBV) infection by maintaining genome integrity and mediating homologous DNA repairs. In this study, 16 sequence variations were detected by resequencing all exons, the exon–intron boundary, and promoter regions of the human RAD51 gene in DNA samples of 24 unrelated individuals. To investigate the association of common variations in the RAD51 locus with HBV infection and hepatocellular carcinoma (HCC) occurrence, six common polymorphisms were genotyped in a total of 1,103 Korean HBV cohort, composed of 433 spontaneously recovered patients as controls and 670 chronic carriers of HBV, who were stratified further into 327 cirrhosis/chronic hepatitis patients and 343 patients with HCC infected with HBV. Logistic analyses revealed no significant association of RAD51 polymorphisms and haplotypes with HBV clearance and HCC occurrence (P > 0.05). Furthermore, with age of infection as an important factor in disease progression to HCC, results from the Cox proportional hazards analysis showed no significant associations between any of the tested RAD51 variants and the age of onset of HCC (P > 0.05), suggesting that genetic polymorphisms of RAD51 may not play an important role in clearance of HBV and disease progression to HCC. Although studies in other populations are needed to confirm these findings, this preliminary data may contribute to the current knowledge on the pathogenesis of hepatitis. J. Med. Virol. 83:1892–1899, 2011. © 2011 Wiley‐Liss, Inc.