The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation

• Published in: Advances in Virology Vol. 2013; no. 2013; pp. 106 - 110
• Main Authors: Moradzadeh, Malihe, Tayebi, Sirous, Poustchi, Hossein, Sayehmiri, Kourosh, Shahnazari, Parisa, Naderi, Elnaz, Montazeri, Ghodratollah, Mohamadkhani, Ashraf
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Limiteds 01.01.2013; Hindawi Puplishing Corporation; Hindawi Publishing Corporation; John Wiley & Sons, Inc; Hindawi Limited; Wiley
• Subjects: Analysis; Biopsy; Colleges & universities; Cytokines; Deoxyribonucleic acid; DNA; Genetic aspects; Hepatitis; Hepatitis B; HIV; Human immunodeficiency virus; Immune system; Infections; Interferon; Ligands; Liver cirrhosis; Measurement; Mutation; Pathogenesis; TLR2
• ISSN: 1687-8639; 1687-8647
• DOI: 10.1155/2013/780319

Recognition mechanisms of innate immune response help to improve immunotherapeutic strategies in HBeAg-negative chronic hepatitis B (CHB). Toll-like receptor 2 (TLR2) is an important component of innate immunity. In this study, the frequency of precore mutations of the hepatitis B virus (HBV) and serum TLR2 were evaluated in CHB patients. Fifty-one patients with chronic hepatitis B, negative for HBeAg and detectable HBV DNA, were examined for the presence of mutations in pre-core region of HBV genome by direct sequencing. Serum TLR2 was measured by enzyme-linked immunosorbent assay. Interactions of truncated HBeAg and TLR2 proteins were evaluated with molecular docking software. The G1896A pre-core mutation were detected in 29 (57%) which was significantly associated with higher concentration of serum TLR2 in comparison with patients without this mutation (4.8 ± 2.9 versus 3.4 ± 2.2 ng/mL, P=0.03). There was also a significant correlation between serum ALT and TLR-2 (r=0.46; P=0.01). Docking results illustrated residues within the N-terminus of truncated HBeAg and TLR2, which might facilitate the interaction of these proteins. These findings showed the dominance of G1896A pre-core mutation of HBV variants in this community which was correlated with serum TLR2. Moreover TLR2 is critical for induction of inflammatory cytokines and therefore ALT elevation.