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Single Nucleotide Polymorphism of the Interferon-γ Gene (IFN-γ +874 T/A) and the Prognosis of Hepatitis B Infection
| Content Provider | Semantic Scholar |
|---|---|
| Author | Naghizadeh, Mohammad Sadegh Naseri, Mohsen Fereyduni, Mohammad Ziaee, Masoud Tane, Abdolghader Safari, Hamidreza Mahavar, Neda Mahdavi, Roya Sarab, Gholamreza Anani |
| Copyright Year | 2018 |
| Abstract | INTRODUCTION Hepatitis B virus (HBV), an enveloped double-stranded DNA virus [1], is the primary cause of acute hepatitis and chronic liver illnesses worldwide, particularly in Asia and Africa [2]. HBV is not cytopathic; some patients become asymptomatic carriers, while others develop liver diseases, such as chronic hepatitis, cirrhosis and hepatocellular carcinoma (HCC) [3, 4]. The pathogenesis of liver disease in chronic HBV infection remains unclear, but the interactions between the host's immune system and the virus ultimately determine the outcome of the disease. The pattern of cytokine production by innate immune cells like the NK cell and the adaptive immune Th1 significantly contribute to the initial control of HBV infection. Interferon-gamma (IFN-γ) is among the principal mediators inducing a host resistance against HBV and the clearance of this virus from hepatocytes [5, 6]. IFN-γ as a proinflammatory Th1 cytokine has a vital role in the antiviral activity, and genetic variation of individuals affects immunity in response to a pathogen [7, 8]. The human IFN-γ gene is located on chromosome 12q24 spanning ~5.4 kb and consists of four exons with three introns [9]. The single nucleotide polymorphism (SNP) of IFN-γ gene +874 A/T (rs2430561) in the first intron is suggested to affect the level of IFN-γ production and thus results in altering the performance of regulatory factors by adjusting their affinities to transcription components [10]. Previous studies investigated the association of 874 T to A transition with several human illnesses, including HBV infection [11]. It is suggested that individuals with T allele at rs2430561 might have an increased level of IFN-γ and the less chance of developing chronic HBV infection [12]. There are reports on variation in genotype and the allele frequencies of cytokine genes in relation to ethnicity and race and the inheritance of particular alleles controlling cytokine production [13, 14]. The Amplification Refractory Mutation System Polymerase Chain Reaction (ARMs-PCR) is a unified DNA amplification-based method used for typing bi-allelic cytokine gene polymorphisms that either directly or indirectly influence gene expression [15]. The object of this study was to highlight the possible relationship between an SNP (rs2430561) in IFN-γ gene Introduction: Chronic Hepatitis B virus infection is a multifactorial disease with a variety of clinical outcomes. Since interferon-gamma (IFN-γ) is a significant immune factor in antiviral defense, this case-control study aimed to investigate the potential relationship between single nucleotide polymorphism of rs2430561 and hepatitis B infection outcome in a population of Birjand city, eastern Iran. Methods: Blood samples were collected from 60 chronically HBVinfected patients and 60 healthy subjects with the history of HBV infection. Genomic DNA was extracted from whole blood by the salting-out method. The first intron of IFN-γ with a length of 264 bp was amplified by Amplification Refractory Mutation System Polymerase Chain Reaction (ARMS-PCR) followed by sequencing. Results: Our results exhibited a statistically significant difference between patients and control individuals (p-value<0.001). The frequency of the allele A was 73.3% in HBVinfected patients, whereas in controls (individuals with a history of HBV infection) it was 46.7%. Conclusion: A statistically significant relationship was found between the IFN-γ (+874T/A, rs2430561) single nucleotide polymorphism (SNP) and chronic HBV infection in the studied population. The obtained results showed that HBV infected individuals with T allele have less risk of progressing to chronic HBV infection. It also suggests that the homozygous carriers of the A allele are more vulnerable to chronic HBV infection. J Med Microbiol Infec Dis, 2018, 6 (2-3): 43-47. |
| Starting Page | 43 |
| Ending Page | 47 |
| Page Count | 5 |
| File Format | PDF HTM / HTML |
| DOI | 10.29252/jommid.6.2.3.43 |
| Volume Number | 6 |
| Alternate Webpage(s) | http://jommid.pasteur.ac.ir/files/site1/user_files_66e506/ghansa-A-10-156-1-d02a814.pdf |
| Alternate Webpage(s) | https://doi.org/10.29252/jommid.6.2.3.43 |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
