Role of tumor necrosis factor gene single nucleotide polymorphisms in the natural course of 2009 influenza A H1N1 virus infection

Antonopoulou, Anastasia; Baziaka, Fotini; Τσαγανός, Θωμάς; Rosario, Maria; Koutoukas, Pantelis; Spyridaki, Aikaterini; Mouktaroudi, Maria; Kotsaki, Antigone; Savva, Athina; Georgitsi, Marianna; Giamarellos‐Bourboulis, Evangelos J.

doi:10.1016/j.ijid.2011.11.012

Cited by 40 publications

(36 citation statements)

References 23 publications

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“…The analysis of the selected SNPs was done using the restriction fragment length polymorphism method. The applied primers and reaction conditions are presented in table 1 [16,17]. Haplotype calculations were done using Unphased [18].…”

Section: Methodsmentioning

confidence: 99%

Impact of TNF Haplotypes in the Physical Course of Acne Vulgaris

et al. 2013

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Background: The role of single-nucleotide polymorphisms (SNPs) of the TNF gene in acne vulgaris remains controversial. Methods: Genomic DNA was isolated from 185 patients with acne vulgaris and 165 healthy controls. SNPs at positions -376, -308 and -238 of the promoter region of TNF were defined. Results: The frequency of the GAG haplotype was greater among patients (16.8%) than among controls with borderline significance (9.7%, p = 0.059). Male carriers of haplotypes other than GGG presented acne vulgaris at a later age than carriers of the GGG haplotype. No effect of the GAG haplotype on the frequency of acne conglobata was found among women with polycystic ovary syndrome. Conclusions: Carriage of the GAG haplotype of TNF is linked with borderline susceptibility to acne vulgaris. The GGG haplotype is related with earlier disease onset in male patients.

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Section: Methodsmentioning

confidence: 99%

Impact of TNF Haplotypes in the Physical Course of Acne Vulgaris

et al. 2013

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“…-238A allele was observed to be significantly higher in 2009 H1N1 cases than controls and carriage of -238A allele was associated with the development of pneumonia [17]. However, these results are specific to a geographic region and have to be confirmed in different cohort.…”

Section: Discussionmentioning

confidence: 81%

“…So far in only one study conducted by Antonopoulou, et al [17] in Greece, role of -238, -308, -376 SNPs in 109 H1N1 infected patients was studied. -238A allele was observed to be significantly higher in 2009 H1N1 cases than controls and carriage of -238A allele was associated with the development of pneumonia [17].…”

Section: Discussionmentioning

confidence: 99%

TNF-Alpha Gene Polymorphism in Indian Population during the Course of Pandemic Influenza a H1N1 Infection: A Pilot Study

Mishra¹

2016

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“…A more recent study found that the lack of Tnf signaling in mice led to increased tissue damage (possibly mediated via MCP-1) during influenza virus infection, even though there was no ultimate difference in clinical outcome [62]. Finally, during the 2009 influenza pandemic, several Tnf associated SNPs identified in human patients were found to be highly correlated with disease severity [63]. Our results show that the replication rates of both X31 and PR8 in the LET-1 cells can be similarly reduced by recombinant Tnf, suggesting that the early induction of Tnf by X31 might contribute to its reduced replication rate in vivo .…”

Section: Discussionmentioning

confidence: 99%

Differential Host Response, Rather Than Early Viral Replication Efficiency, Correlates with Pathogenicity Caused by Influenza Viruses

et al. 2013

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Influenza viruses exhibit large, strain-dependent differences in pathogenicity in mammalian hosts. Although the characteristics of severe disease, including uncontrolled viral replication, infection of the lower airway, and highly inflammatory cytokine responses have been extensively documented, the specific virulence mechanisms that distinguish highly pathogenic strains remain elusive. In this study, we focused on the early events in influenza infection, measuring the growth rate of three strains of varying pathogenicity in the mouse airway epithelium and simultaneously examining the global host transcriptional response over the first 24 hours. Although all strains replicated equally rapidly over the first viral life-cycle, their growth rates in both lung and tracheal tissue strongly diverged at later times, resulting in nearly 10-fold differences in viral load by 24 hours following infection. We identified separate networks of genes in both the lung and tracheal tissues whose rapid up-regulation at early time points by specific strains correlated with a reduced viral replication rate of those strains. The set of early-induced genes in the lung that led to viral growth restriction is enriched for both NF-κB binding site motifs and members of the TREM1 and IL-17 signaling pathways, suggesting that rapid, NF-κB –mediated activation of these pathways may contribute to control of viral replication. Because influenza infection extending into the lung generally results in severe disease, early activation of these pathways may be one factor distinguishing high- and low-pathogenicity strains.

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Role of tumor necrosis factor gene single nucleotide polymorphisms in the natural course of 2009 influenza A H1N1 virus infection

Abstract: The -238 A SNP allele of the TNF gene imposes on the course of 2009 H1N1 virus infection and is an independent risk factor for pneumonia.

Cited by 40 publications

References 23 publications

Impact of TNF Haplotypes in the Physical Course of Acne Vulgaris

Impact of TNF Haplotypes in the Physical Course of Acne Vulgaris

TNF-Alpha Gene Polymorphism in Indian Population during the Course of Pandemic Influenza a H1N1 Infection: A Pilot Study

Differential Host Response, Rather Than Early Viral Replication Efficiency, Correlates with Pathogenicity Caused by Influenza Viruses

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