The association of variations in TLR genes and spontaneous immune control of hepatitis B virus - 03/04/18
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Highlights |
Toll-like receptors (TLRs) are important for chronic hepatitis B progression. This study showed the association of TLRs and hepatitis B virus (HBV) chronicity. In future, these polymorphisms may be clinically used to determine the risk of a chronic HBV infection.
Le texte complet de cet article est disponible en PDF.Summary |
Background |
Toll-like receptors (TLRs) are suspected to play a critical role in liver diseases and the progression of chronic hepatitis B (CHB) infection. In this study, we investigated the possible association between TLRs and hepatitis B virus (HBV) infection chronicity in Turkish population.
Methods |
TLR4 (+896 A→G) (rs4986790), TLR5 (+1846 T→C) (rs5744174) and TLR9 (−1237T→C) (rs5743836) polymorphisms were screened in 131 CHB patient and 168 individuals by polymerase chain reaction (PCR) – restriction fragment length polymorphism (RFLP) technique.
Results |
Of the screened polymorphisms, TT genotype of the missense variant TLR5 (rs5744174) (NM_003268.5:c.1846T>C (p.Phe616Leu) is significantly more frequent in the control group than CHB patients (P<0.001), presence of TT genotype of the upstream variant TLR9 (rs5743836) (NM_017442.3:c.−1237T>C) is more frequent in CHB group (P=0.043). However, no significant association was found for the missense variant TLR4 (rs4986790) NM_138554.4:c.896A>G (p.Asp299Gly) polymorphism and CHB in Turkish population.
Conclusions |
From all three analyzed SNPs association of TLR5 (rs5744174) with CHB is the most significant. Since TLR5 is associated with interferon-γ production, a high frequency of TT at rs5744174 in controls subjects suggests that it represents a protective genotype against CHB plausibly associated with an increased interferon-γ production.
Le texte complet de cet article est disponible en PDF.Keywords : Toll-like receptors, Chronic hepatitis B, Seroconversion, Polymorphism, PCR-RFLP
Plan
Vol 42 - N° 2
P. 139-144 - avril 2018 Retour au numéro
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