Hepatitis B virus (HBV) is the one of the major causes of chronic liver disease. Individuals exposed to HBV show wide spectrum outcomes including immunized persons, asymptomatic carrier, chronic active hepatitis, cirrhosis and HCC. The outcome of HBV infection and the severity of associated liver diseases are determined by the nature and strength of host immune responses against the virus. There is accumulating evidence that the innate branch of the host immune system plays an important role in the control of HBV infection. Various components, such as natural killer (NK) cells, natural killer T (NKT) cells, dendritic cells, cytokines, chemokines and toll-like receptor (TLR) contribute to this nonspecific innate immune response .TLR3 play an important role in innate immune response against viral pathogens. Single nucleotide polymorphisms (SNPs) in the TLR3 could be considered as factors for the susceptibility to viral pathogens including HBV. This study aimed to investigate the distribution of six SNPs of the TLR3 gene in patients infected with HBV and to study the relation between these SNPs and the clearance of hepatitis B virus. These SNPs were tested by direct sequencing. Three groups were investigated: chronic HBV carrier (25 patients), chronic active HBV carrier (16 patients) and 13 persons who are previously exposed to HBV and become immunized. These 3 groups were examined for six SNPs (rs5743311, rs5743312, rs5743313, rs5743314, rs5743315, and rs78726532). The analysis confirmed that GCTCCA haplotype and CCA haplotype showed significant higher frequency in immunized group when compared to chronic hepatitis B groups. These findings indicate that genetic variations in the TLR3 gene could affect the outcome of HBV infection.
Research Department	
              
          Research Journal	
              Egyptian journal of immunology
          Research Member	
          
      Research Publisher	
              NULL
          Research Rank	
              2
          Research Vol	
              NULL
          Research Website	
              NULL
          Research Year	
              2017
          Research_Pages	
              NULL
          Research Abstract	
              
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