A genome-wide association study of hepatitis B vaccine response in an Indonesian population reveals multiple independent risk variants in the HLA region

Png, Eileen; Thalamuthu, Anbupalam; Ong, Rick Twee Hee; Snippe, H.; Boland, Greet J.; Seielstad, Mark

doi:10.1093/hmg/ddr302

Cited by 111 publications

(101 citation statements)

References 16 publications

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“…Recently the importance of HLA genes was further highlighted by the first genome-wide association study (GWAS) in Asian patients with chronic hepatitis B, where HLA-DP gene variation showed the strongest association with chronic HBV infection (8), which was validated subsequently in another Asian study (4). This variant also associated with HBV vaccination response in Asians (18). HLA-DP is an HLA class II heterodimeric molecule consisting of alpha and beta chains that are encoded by the HLA-DPA1 and -DPB1 genes, respectively.…”

mentioning

confidence: 95%

A Novel Variant Marking HLA-DP Expression Levels Predicts Recovery from Hepatitis B Virus Infection

Thomas

Thio

Apps

et al. 2012

J Virol

147

186

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:01), whereas 550A/G does not. 496A/G has a stronger effect than any individual HLA-DPB1 or DPA1 allele and any other HLA alleles that showed an association with HBV recovery in our European-American cohort. The 496GG genotype, which confers recessive susceptibility to HBV persistence, also associates in a recessive manner with significantly higher levels of HLA-DP surface protein and transcript level expression in healthy donors, suggesting that differences in expression of HLA-DP may increase the risk of persistent HBV infection.

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mentioning

confidence: 95%

A Novel Variant Marking HLA-DP Expression Levels Predicts Recovery from Hepatitis B Virus Infection

Thomas

Thio

Apps

et al. 2012

J Virol

147

186

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“…Several studies, especially analyzing Asian samples, found association between the SNP rs9277535 and chronic HBV infection (Kamatani et al, 2009;Lau et al, 2011;Mbarek et al, 2011;Png et al, 2011;Nishida et al, 2012;Yan et al, 2012;Kim et al, 2013;Al-Qahtani et al, 2014;Chang et al, 2014;Liao et al, 2014;Pan et al, 2014;He et al, 2015;Yu et al, 2015). Additionally, the study conducted by Thomas et al (2012) found an association between the SNP rs9277535 and the elimination rate of HBV in patients EuroAmerican and African-Americans (P = 0.0001).…”

Section: Discussionmentioning

confidence: 98%

Lack of association between human leukocyte antigen polymorphisms rs9277535 and rs7453920 and chronic hepatitis B in a Brazilian population

Pereira¹,

Wolf²,

Stumm³

et al. 2017

Genet. Mol. Res.

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ABSTRACT. Hepatitis B virus (HBV) infection is a serious public health problem worldwide. The progression of the disease depends on several host and viral factors and may result in fulminant hepatitis (very rare), acute hepatitis with spontaneous clearance, and chronic hepatitis B infection. Previous studies demonstrated that variations in the human leukocyte antigen (HLA) class II (HLA-DPB1 and HLA-DQB2 genes) are related to the chronic HBV infection. This study aimed to investigate the association of two single nucleotide polymorphism (SNPs), one in the HLA-DPB1 (rs9277535) and one in the HLA-DQB2 (rs7453920), with chronic hepatitis B infection in a southern Brazilian sample. This case-control study included 260 HBV patients attended in a Specialized 2 V.R.Z.B. Pereira et al. Genetics and Molecular Research 16 (2): gmr16029565Center for Health in Caxias do Sul (Brazil) between 2014 and 2016. The same number of controls (matching for age, gender, and ethnicity) was obtained in a University Hospital in the same city and period. Blood samples were collected and genomic DNA was extracted. Genotyping were performed by real-time Taqman PCR method. Odds ratios with 95% confidence intervals and significance level of 5% (P < 0.05) were calculated. Allele frequencies in the SNP rs9277535 were 72.6% for A and 27.4% for G nucleotides in cases and 75.0% for A and 25.0% for G in controls. Allele frequencies in the SNP rs7453920 were of 25.7% for A and 74.3% for G in cases and 28.8% for A and 71.2% for G in controls. No statistically significant association was found between both SNPs and chronic hepatitis B (P > 0.05).

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“…As described above, the HLA-II genetic polymorphisms are statistically associated with the outcomes of exposureto HBV [18][19][20][21][22][23][24][25][26][27] . This genetic background may predispose immune imbalance upon HBV infection.…”

Section: Interaction Of Genetic Predispositions Of Immune or Inflammamentioning

confidence: 93%

“…Genome-wide association study in the eastern Asian populations have shown that a total of 11 single nucleotide polymorphisms (SNPs) in genetic loci including HLA-DPA1 and HLA-DPB1, some SNPs in genetic loci including HLA-DQ and -DR, and a locus near HLA-Care significantly associated with CHB [18][19][20][21][22] . Interestingly, these SNPs in the loci encoding human leukocyte antigen-class II (HLA-II) are also significantly associated with vaccine response as well as the risks of acute-on-chronic liver failure, HBVrelated liver cirrhosis, and HBV-associated HCC [23][24][25][26][27] . Interestingly, different human races have different allelic frequencies of SNPs that affect the expression of HLA-DP, HLA-DQ, and the inhibitory component of NF-κB complex IκBa gene NFKBIA.…”

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confidence: 99%

Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis

Cao¹

2017

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How to cite this article: Cao GW. Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis. Hepatoma Res 2017;3:241-59.Non-resolving inflammation, which may be maintained by infection, pollution, and metabolic stimulants and their interactions with immunogenetic predisposition, provides a fertile field for cancer development. This is strongly evident in hepatocellular carcinoma. Here, the framework of a hypothesis called Cancer Evo-Dev is presented, based on the advances in hepatitis B virusinduced hepatocarcinogenesis. Several aspects central to this theory are as follows: (1) immune imbalance caused by the interaction of immunogenetic predispositions and hepatitis B virus infection maintains non-resolving inflammation; (2) active inflammation executants promote mutations in viral and host genomes via disbalancing mutagenic forces including cytidine deaminases and mutation-repairing forces including uracil-DNA glycosylases, thus promoting cancer-related somatic mutations and viral mutations; (3) a small percentage of the cells whose somatic mutations alter the survival signalling adapt to the inflammatory microenvironment, de-differentiate via demethylating role of cytidine deaminases, and reversely develop into tumor-initiating cells (TICs); (4) under the cultivation of some factors like POSTN from tumorinfiltrating fibroblasts and M2 macrophages, TICs acquire the stemness, cancer-stem cells obtain distinct metastatic and drug-resistant potentials under the selection pressure from distinct microenvironments; (5) glycolysis persistence in the presence of oxygen provides essential energy for cell survival and the raw material for DNA synthesis. Thus, cancer development is characterized by an evolutionary process of "mutation-selection-adaptation". The framework of Cancer Evo-Dev can be verified in other cancers. Cancer Evo-Dev lays theoretical foundation for understanding the mechanisms by which inflammation promotes cancer development, and it also plays a role in specific prophylaxis, prediction, and targeted treatment of cancers. Key words:Inflammation, hepatitis B virus, mutations, hepatoma, Cancer Evo-Dev ABSTRACTArticle history:

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A genome-wide association study of hepatitis B vaccine response in an Indonesian population reveals multiple independent risk variants in the HLA region

Cited by 111 publications

References 16 publications

A Novel Variant Marking HLA-DP Expression Levels Predicts Recovery from Hepatitis B Virus Infection

A Novel Variant Marking HLA-DP Expression Levels Predicts Recovery from Hepatitis B Virus Infection

Lack of association between human leukocyte antigen polymorphisms rs9277535 and rs7453920 and chronic hepatitis B in a Brazilian population

Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis

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