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

Summary Objectives To identify the role of single nucleotide polymorphisms (SNPs) of the tumor necrosis factor (TNF) gene in the natural course of 2009 influenza A H1N1 virus infection. Methods Genomic DNA was isolated from 109 patients with an H1N1 infection and from 108 healthy volunteers. SNPs of the TNF gene were assessed after electrophoresis of the digested PCR products by restriction enzymes. Results The frequency of the −238 A allele was significantly greater among patients than among controls. Viral pneumonia developed in 20 of 96 non-carriers of at least one −238 A allele (20.8%) and in seven of 13 carriers of at least one −238 A allele (53.8%, p =0.016). Logistic regression analysis showed that the most important factors associated with the development of pneumonia were the presence of an underlying disease ( p =0.021, odds ratio (OR) 3.08) and the carriage of at least one −238 A allele ( p =0.041, OR 3.74). Gene transcripts of the TNF gene were greater among non-carriers of the −238 A allele than among carriers of the −238 A allele. Conclusions 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.