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Evaluation of death pathway genes FAS and FASL polymorphisms in chronic HBV infection
Author(s) -
Zamani A. G.,
Barlas I. O.,
DurakbasiDursun G.,
Ural O.,
Erdal E.,
Yildirim M. S.
Publication year - 2013
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/iji.12056
Subject(s) - fas ligand , genotype , restriction fragment length polymorphism , hepatitis b virus , allele , gene , immunology , apoptosis , polymorphism (computer science) , biology , virology , virus , microbiology and biotechnology , genetics , programmed cell death
Summary This study was designed to determine the possible asssociation between selected FAS and FASLG polymorphisms and Hepatitis B virus ( HBV ) infection. FAS ‐670 G/A, FAS ‐1377 G/A, FASLG ‐844 T/C and FASLG IVS 2nt‐124 A/G polymorphisms were genotyped by polymerase chain reaction and restriction fragment length polymorphism ( PCR ‐ RFLP ). A total of age and sex matched 108 controls and a hundred chronic HBV patients were recruited to conduct a case–control study. FAS ‐670 polymorphism was associated with chronic HBV infection ( P = 0.03) FAS ‐ 1377 GG , GA and AA genotypes among the cases (90%, 5% and 5%, respectively) were significantly different from those among the controls (68%, 31.5% and 5.6%; P = 0.00). FASLG ‐844 allele distribution was similar between the groups ( P = 0.17) but TC genotype (67.3%) was frequent in chronic HBV patients, while CC genotype was found significantly higher (29.6%) in controls. No association between FASLG IVS 2nt‐124 polymorphism and chronic HBV infection could be identified ( P = 0.55). FAS ‐670 polymorphism is associated with chronic HBV infection, while FASLG IVS 2nt‐124 A/G polymorphism is not. The FAS ‐1377G/A and FASLG ‐ 844 T/C genotypes are likely to play a substantial role in HBV infection. Further studies evaluating polymorphisms in other genes related with apoptosis are needed to elucidate the role of genetic variation in HBV infection.