Advances in the genome-wide association study of chronic hepatitis B susceptibility in Asian population

Qiu, Bing; Jiang, Wei; Olyaee, Mojtaba; Sakai, Kenji; Miyakawa, Akihiro; Hu, Huijing; Zhu, Yi; Tang, Lihong

doi:10.1186/s40001-017-0288-3

Cited by 7 publications

(6 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, the IL1B rs16944 allele C has been identified as a genetic marker for the development of hepatocarcinoma in patients with chronic HBV infection [ 31 ]. Furthermore, genome-wide association study in southwest China revealed 6 new loci, including the rs16944 SNP in the IL1B gene, associated with an increased prevalence rate of chronic hepatitis B [ 32 ]. Altogether, the rs16944 may be a genetic modifier of hepatitis caused by either HBV or HCV.…”

Section: Discussionmentioning

confidence: 99%

Inflammasome genes polymorphisms may influence the development of hepatitis C in the Amazonas, Brazil

et al. 2021

View full text Add to dashboard Cite

Hepatitis C is considered a major public health problem caused by the hepatitis C virus (HCV). Viral infections are known to induce production of IL1β through the signaling pathway of inflammasomes. Emerging evidences suggest that Inflammasome genes may influence the immune response against HCV as the host genetic background may contribute to the balance between acute and chronic inflammation. We investigated in 151 patients with chronic hepatitis C and 206 healthy blood donors’ individuals (HD). Polymorphisms in the IL1B and IL18 genes were genotyped by PCR-RFLP, while NLRP3, CARD8, CTSB and AIM2 by RT- PCR. Serum assay of IL-1β cytokine was performed by ELISA. 84 patients presented mild fibrosis (<F2) and 67 advanced fibrosis (≥ F2). Among the HD individuals the NLRP3-rs10754558 C/C genotype correlated with higher IL-1β levels compared to the G/G genotype. Similar pattern was observed in patients with hepatitis C, mean circulating IL-1β levels were 21,96 ± 4.5 and 10,62 ± 3.3pg/mL among the C/C and G/G genotypes, respectively. This pattern holds even after stratification of the patients into mild fibrosis and advanced fibrosis, demonstrating that the NLRP3-rs10754558 or another polymorphism in linkage disequilibrium with it possibly has an influence on the processing of pro-IL-1β. Notably, higher levels of IL-1β (Mann–Whitney test, p<0.0001) were observed among patients (mean ± SEM: 19,24 ±3.pg/mL) when compared with controls (mean ± SEM: 11,80 ±1.0pg/mL). Gene-gene interaction showed that individuals heterogyzotes for both CARD8-rs2009373 and IL1B-rs16944 are less prone to hepatitis C development (padj = 0.039). Similarly, herozygote carriers for CTSB-rs1692816 and AIM2-rs1103577 (padj = 0.008) or for IL18-rs187238 and NLRP3-rs10754558 (padj = 0.005), have less chances to the development of hepatitis C. However, between subgroups of <F2 and ≥F2, individuals homozygous for the T allele of CARD8-rs2009373 and heterozygous for IL18-rs187238 (padj = 0.028), have mild form of fibrosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Inflammasome genes polymorphisms may influence the development of hepatitis C in the Amazonas, Brazil

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Several studies have identified single nucleotide polymorphisms (SNPs) in human leukocyte antigens (HLA) that have been associated with the outcome of HBV infection, either with clearance or progression of chronic infection, although some findings were not subsequently supported in other manuscripts. Among the more in depth characterized, it has been found that HLA-DP (rs3077 and rs9277535) and HLA-DQ (rs7453920 and rs2856718) SNPs were associated to HBV persistence[ 25 - 27 ] Notably, different studies have also identified several HLA polymorphisms associated with the response to the HBV vaccine[ 28 , 29 ]. Additionally, it was also reported that cytokine, chemokine, toll like receptor, sodium taurocholate cotransporting polypeptide, and vitamin D-related genes may influence the clinical outcomes of HBV infection[ 24 , 30 , 31 ].…”

Section: Hepatitis B Virusmentioning

confidence: 99%

Viral hepatitis update: Progress and perspectives

Pisano¹,

Giadans²,

Flichman³

et al. 2021

WJG

View full text Add to dashboard Cite

Viral hepatitis, secondary to infection with hepatitis A, B, C, D, and E viruses, are a major public health problem and an important cause of morbidity and mortality. Despite the huge medical advances achieved in recent years, there are still points of conflict concerning the pathogenesis, immune response, development of new and more effective vaccines, therapies, and treatment. This review focuses on the most important research topics that deal with issues that are currently being solved, those that remain to be solved, and future research directions. For hepatitis A virus we will address epidemiology, molecular surveillance, new susceptible populations as well as environmental and food detections. In the case of hepatitis B virus, we will discuss host factors related to disease, diagnosis, therapy, and vaccine improvement. On hepatitis C virus, we will focus on pathogenesis, immune response, direct action antivirals treatment in the context of solid organ transplantation, issues related to hepatocellular carcinoma development, direct action antivirals resistance due to selection of resistance-associated variants, and vaccination. Regarding hepatitis D virus, we describe diagnostic methodology, pathogenesis, and therapy. Finally, for hepatitis E virus, we will address epidemiology (including new emerging species), diagnosis, clinical aspects, treatment, the development of a vaccine, and environmental surveillance.

show abstract

“…16 A number of CHB-related susceptibility loci and genetic regions have been reported, among which 26 important candidate single-nucleotide polymorphisms (SNPs) were identified. 17 Therefore, the variations caused by SNPs that affect expression of cytokines that regulate and initiate the immune system such as IL-12B may reduce the ability of the immune system to elicit a response against viral infections. 18 The active cytokine is a 70 kDa heterodimer comprising two covalently linked proteins of 35 kDa (p35) and 40 kDa (p40) 19 ; each subunit is encoded on different chromosomes.…”

Section: Introductionmentioning

confidence: 99%

Strong association of functional polymorphism in IL‐12B with susceptibility to chronic hepatitis B in Tunisia

Dhifallah

Ayouni

Jmel

et al. 2021

Journal of Medical Virology

View full text Add to dashboard Cite

Background The chronicity or clearance of hepatitis B virus (HBV) infection depends on viral and genetic variables. The immune response against HBV is thought to be responsible for viral persistence or clearance. Cytokines such as interleukin 1‐2B (IL1‐2B) involved in the T‐helper 1 system are key mediators in the defence mechanisms against viral infection and play a role in the regulation of HBV clearance during infection. We aimed to examine whether the polymorphic variant TaqI polymorphism in the 3′‐untranslated region (3′‐UTR; rs3212227) suspected to modulate interleukin‐levels of IL‐12B has an influence on the risk of development of chronicity after HBV exposure. Methods Genotyping was performed by the polymerase chain reaction‐restriction fragment length polymorphism method for 236 patients with chronic hepatitis B (CHB) and 240 controls from different cities of Tunisia recruited in the Pasteur Institute of Tunisia between January 2017 and December 2018. Results We found that the IL‐12B polymorphism was associated with a significantly increased risk of CHB in patients (p = 1 × 10−3; χ 2 = 10.31 and odds ratio [OR] = 2.14; 95% confidence interval [CI] = 1.30–3.52) when AC/CC variant genotypes were compared with the wild‐type AA homozygote. Statistical significance was found when CHB‐males were compared with CHB‐females (p = 2 × 10−7; χ 2 = 26.62 and p = 1 × 10−3; χ 2 = 10.36, for genotypic and allelic frequencies, respectively). Also, CHB‐patients carrying C‐allele less than 50‐years were at an increased risk of developing chronic HBV infection than patients more than 50‐years (p = 6.1 × 10−5; χ 2 = 16.07). Conclusions These results suggest that the C‐allele would affect susceptibility to chronicity after HBV exposure in Tunisian patients especially for males less than 50‐years. Age and sex have an influence on this polymorphism in CHB Tunisian patients.

show abstract

Advances in the genome-wide association study of chronic hepatitis B susceptibility in Asian population

Cited by 7 publications

References 32 publications

Inflammasome genes polymorphisms may influence the development of hepatitis C in the Amazonas, Brazil

Inflammasome genes polymorphisms may influence the development of hepatitis C in the Amazonas, Brazil

Viral hepatitis update: Progress and perspectives

Strong association of functional polymorphism in IL‐12B with susceptibility to chronic hepatitis B in Tunisia

Contact Info

Product

Resources

About