Relationship between programmed cell death-1 polymorphisms and clearance of hepatitis B virus.
Programmed cell death-1 (PD-1) plays a critical role in regulating T-cell function during hepatitis B virus (HBV) infection. This study investigated the relationship between the polymorphisms of PD-1 gene and the susceptibility to HBV infection. Single nucleotide polymorphisms (SNPs) in PD-1 gene at positions +7146 G>A (guanine to adenine substitution) and +7209 C>T (cytosine to thymine substitution) were analysed using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method in 220 subjects with chronic hepatitis B infection and 165 spontaneous clearance of HBV subjects. However, no statistically significant differences were found in the genotype distributions of the PD-1 +7146 G>A and PD-1 +7209 C>T polymorphisms among chronic hepatitis B and spontaneous clearance subjects. According to stratified analyses, borderline significance was observed between PD-1 +7146 GA genotype and risk of HBV chronicity in the subgroup of male gender (OR = 1.88, 95% 0.95-3.71; P = 0.07). Our findings demonstrate for the first time that the PD-1 +7146 G>A and PD-1 +7209 C>T polymorphisms have not been any major role in genetic susceptibility to chronicity of HBV infection, at least in the population studied here. Independent studies are needed to validate our findings in a larger series, as well as in patients of different ethnic origins.
Department of Gastroenterology, Faculty of Medicine, Çukurova University, Adana, Turkey.
Y
Y
Ülger
Department of Nursing, Adıyaman School of Health, Adıyaman University, Adıyaman, Turkey.
S
S
Bayram
Department of Gastroenterology, Faculty of Medicine, Çukurova University, Adana, Turkey.
M Ü
MÜ
Sandıkçı
Department of Gastroenterology, Faculty of Medicine, Çukurova University, Adana, Turkey.
E
E
Akgöllü
Department of Gastroenterology, Faculty of Medicine, Çukurova University, Adana, Turkey.
A
A
Bekar
D000328:Adult; D000483:Alleles; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006239:Haplotypes; D006509:Hepatitis B / Q000097:blood / Q000235:genetics* / Q000276:immunology* / Q000821:virology; D006510:Hepatitis B Antibodies / Q000097:blood / Q000276:immunology; D006514:Hepatitis B Surface Antigens / Q000097:blood / Q000276:immunology; D006513:Hepatitis B e Antigens / Q000097:blood / Q000276:immunology; D006515:Hepatitis B virus / Q000276:immunology*; D019694:Hepatitis B, Chronic / Q000235:genetics / Q000276:immunology / Q000821:virology; D006801:Humans; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D020641:Polymorphism, Single Nucleotide; D061026:Programmed Cell Death 1 Receptor / Q000235:genetics*; D019562:Viral Load
D006510:Hepatitis B Antibodies; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D061026:Programmed Cell Death 1 Receptor