A Functional Variation in CD55 Increases the Severity of 2009 Pandemic H1N1 Influenza A Virus Infection

Zhou, Jie; To, Kelvin Kai-Wang; Dong, Hui; Cheng, Zhongshan; Lau, Candy C. Y.; Poon, Vincent Kwok Man; Fan, Yanhui; Song, You‐Qiang; Tse, Herman; Chan, Kwok‐Hung; Zheng, Bo‐Jian; Zhao, Guoping; Yuen, Kwok‐Yung

doi:10.1093/infdis/jis378

Cited by 86 publications

(86 citation statements)

References 35 publications

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“…DAF rs2564978 T > C polymorphism is located in the promoter of DAF. Evidences have demonstrated that the carriers with DAF rs2564978 C allele exhibited significantly higher DAF mRNA expression levels on moncytes that those with TT genotype (Zhou et al, 2012). In our present study, we genotyped the DAF rs2564978 polymorphism among our case-control population and found that CC genotype carriers had marginally significant association with gastric cancer risk compared with TT genotype carriers with OR (95% CI) of 1.42(0.99-2.05) (P = 0.058).…”

Section: Discussionmentioning

confidence: 99%

The tag SNP rs10746463 in decay-accelerating factor is associated with the susceptibility to gastric cancer

Song

Zhi

Liu

et al. 2015

Molecular Immunology

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Section: Discussionmentioning

confidence: 99%

The tag SNP rs10746463 in decay-accelerating factor is associated with the susceptibility to gastric cancer

Song

Zhi

Liu

et al. 2015

Molecular Immunology

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“…A SNP in CD55 , rs2564978, was chosen from 5,166 SNPs identified by a small-scale GWAS study in 25 Chinese patients with severe influenza and 26 controls [106]. This SNP caused reduced expression of CD55 (also known as decay accelerating factor, DAF), which can reduce epithelial cell damage during influenza infection [106]. A similar GWAS study of 42 Chinese patients with severe pH1N1 or H7N9 infection and 42 controls crossed with a quantitative cis-QTL study in the lung yielded 1,114 SNPs.…”

Section: Introductionmentioning

confidence: 99%

Host genetics of severe influenza: from mouse Mx1 to human IRF7

Ciancanelli

Abel

Zhang

et al. 2016

Current Opinion in Immunology

109

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Influenza viruses cause mild to moderate respiratory illness in most people, and only rarely devastating or fatal infections. The virulence factors encoded by viral genes can explain seasonal or geographic differences at the population level but are unlikely to account for inter-individual clinical variability. Inherited or acquired immunodeficiencies may thus underlie severe cases of influenza. The critical role of host genes was first demonstrated by forward genetics in inbred mice, with the identification of interferon (IFN)-α/β-inducible Mx as a canonical influenza susceptibility gene. Reverse genetics has subsequently characterized the in vivo role of other mouse genes involved in IFN-α/β and –λ immunity. A series of in vitro studies with mouse and human cells have also refined the cell-intrinsic mechanisms of protection against influenza viruses. Population-based human genetic studies have not yet uncovered variants with a significant impact. Interestingly, human primary immunodeficiencies affecting T and B cells were also not found to predispose to severe influenza. Recently however, human IRF7 was shown to be essential for IFN-α/β- and IFN-λ-dependent protective immunity against primary influenza in vivo, as inferred patient with life-threatening influenza revealed to be IRF7-deficient by whole exome sequencing. Next generation sequencing of human exomes and genomes will facilitate the analysis of the human genetic determinism of severe influenza.

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“…Several potential genetic determinants associated with A(H1N1)pdm09 infection have been described, including TNF (Antonopoulou et al, 2012), IFN-inducible transmembrane (Everitt et al, 2012), killer-cell immunoglobulin-like receptor (Aranda-Romo et al, 2012), complement regulatory protein CD55 (Zhou et al, 2012) and Toll-like receptor 3 (Esposito et al, 2012). Data relating to the role of chemokine receptor 5 (CCR5) in severe A(H1N1)pdm09-infected patients are contradictory and have been debated (Keynan et al, 2010;Rodriguez et al, 2013;Sironi et al, 2014).…”

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confidence: 99%

CCR5 deficiency predisposes to fatal outcome in influenza virus infection

Falcón

Cuevas

Rodríguez-Frandsen

et al. 2015

Journal of General Virology

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Influenza epidemics affect all age groups, although children, the elderly and those with underlying medical conditions are the most severely affected. Whereas co-morbidities are present in 50 % of fatal cases, 25-50 % of deaths are in apparently healthy individuals. This suggests underlying genetic determinants that govern infection severity. Although some viral factors that contribute to influenza disease are known, the role of host genetic factors remains undetermined. Data for small cohorts of influenza-infected patients are contradictory regarding the potential role of chemokine receptor 5 deficiency (CCR5-D32 mutation, a 32 bp deletion in the CCR5 gene) in the outcome of influenza virus infection. We tested 171 respiratory samples from influenza patients (2009 pandemic) for CCR5-D32 and evaluated its correlation with patient mortality. CCR5-D32 patients (17.4 %) showed a higher mortality rate than WT individuals (4.7 %; P50.021), which indicates that CCR5-D32 patients are at higher risk than the normal population of a fatal outcome in influenza infection. Influenza A viruses are a major source of acute respiratory infections and continue to be an important cause of acute illness and death worldwide. They cause annual epidemics and occasional pandemics with potentially fatal outcome. The mean global burden of seasonal influenza is more than 600 million cases, with 3 million cases of severe illness and almost 500 000 deaths per year worldwide (http://www. who.int/en/). A new H1N1 subtype influenza A virus emerged in 2009 [A(H1N1)pdm09], which was highly transmissible with relatively low virulence and caused the first pandemic of the 21st century (Neumann et al., 2009).Differences in disease severity can be due to pre-existing health conditions, predisposing host genetic factors, differences in the virulence of circulating viruses or a combination of these factors. The co-morbid conditions for A(H1N1)pdm09 include chronic metabolic disease, primarily diabetes mellitus and renal disease, chronic lung and cardiac disease, immunosuppressive conditions, neoplasms, obesity and pregnancy (Falagas et al., 2011; Louie et al., 2011;Singanayagam et al., 2011).Although co-morbidities are present in half of fatal cases, one-third of fatal cases have no co-morbid conditions (http://www.cdc.gov/h1n1flu/estimates_2009_h1n1.htm), suggesting that host genetic variation accounts for the distinct disease severity of A(H1N1)pdm09 infection. Several potential genetic determinants associated with A(H1N1)pdm09 infection have been described, including TNF (Antonopoulou et al., 2012), IFN-inducible transmembrane (Everitt et al., 2012), killer-cell immunoglobulin-like receptor (Aranda-Romo et al., 2012), complement regulatory protein CD55 (Zhou et al., 2012) and Toll-like receptor 3 (Esposito et al., 2012). Data relating to the role of chemokine receptor 5 (CCR5) in severe A(H1N1)pdm09-infected patients are contradictory and have been debated (Keynan et al., 2010;Rodriguez et al., 2013;Sironi et al., 2014).CCR5 regulates various aspec...

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A Functional Variation in CD55 Increases the Severity of 2009 Pandemic H1N1 Influenza A Virus Infection

Cited by 86 publications

References 35 publications

The tag SNP rs10746463 in decay-accelerating factor is associated with the susceptibility to gastric cancer

The tag SNP rs10746463 in decay-accelerating factor is associated with the susceptibility to gastric cancer

Host genetics of severe influenza: from mouse Mx1 to human IRF7

CCR5 deficiency predisposes to fatal outcome in influenza virus infection

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