Analysis of Hepatitis B virus (HBV) mutations in patients from Western Saudi Arabia with chronic disease

肝细胞癌 乙型肝炎病毒 基因型 医学 肝病 胃肠病学 病毒学 乙型肝炎 内科学 慢性肝病 神秘的 纤维化 病毒 生物 病理 基因 遗传学 肝硬化 替代医学
作者
Sherif A. El‐Kafrawy,Ghazi A. Jamjoom,Hisham Othman Akbar,Hind I Fallatah,Maï El-Daly,Yousef Qari,Abdullah S Alghamdi,Mohammed A. Babatin,Mohammed Alsaedi,Noura A. Othman,Tagreed L. Alsubhi,Mohamed Abdel‐Hamid,Esam I. Azhar
出处
期刊:Journal of Infection in Developing Countries [Open Learning on Enteric Pathogens]
卷期号:12 (07): 557-567
标识
DOI:10.3855/jidc.9534
摘要

Introduction: Extensive research has provided a link between HBV variants and the clinical complications of liver diseases. This study was performed to further investigate the relationship between HBV variants in preS, S and BCP/PC regions and disease progression in chronic hepatitis B (CHB) cases in Jeddah, Saudi Arabia. Methodology: 182 CHB patients were recruited for this study. HBV DNA was amplified by PCR in the PreS, S, and BCP/PC regions. Sequences were generated from 31 and 26 treated cases in PreS and S regions respectively and from 72 cases in the BCP/PC region. Results: The majority of cases (86.7%) were genotype D. Mutations at preS1-A2922C, X-A1624C and PC-G1887A were detected only in cases with either a high fibrosis score or hepatocellular carcinoma (HCC), while mutations at positions PC-C1982A, PC-G1951T, X-C1628T and X-A1630G were detected more frequently in HCC cases, without reaching statistical significance. Seven deletions were detected in the PreS-region. No deletions were detected in the CCAAT box. The accumulation of mutations per sample in the preS1-2 and S regions were associated with elevated ALT (p < 0.001, 0.001 and 0.001; respectively) and increased fibrosis (p = 0.018, 0.02 and 0.013; respectively). The accumulation of mutations per sample in the BCP/PC region is associated with high viral load. Occult hepatitis B infection (OBI) was identified in 5 samples. Conclusion: Our results add to the knowledge about HBV genotype-D variants. The accumulation of mutations per sample and OBI seem to play a role in the progression of HBV infection. G1896A was associated with the HBeAg negativity. The preS deletions did not play a role in liver disease progression.

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