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BMC Res Notes. 2014; 7: 504.

Abstract

Background

Host genetic factors are thought to modulated the severity of disease caused by infection with the 2009 H1N1 pandemic influenza virus (H1N1pdm09). The human CCR5 gene encodes a cytokine receptor important for cell-mediated immune response against H1N1pdm09. A 32-bp polymorphic deletion in the coding sequence of CCR5, the so-called CCR5Δ32 allele, segregates in populations of European ancestry with a frequency of 8-15%. A high proportion of CCR5Δ32 heterozygotes was reported in a sample of white Canadian critically-ill H1N1pdm09 infected subjects, suggesting an association with disease severity.

Methods

We recruited 29 H1N1pdm09 infected subjects from Southern Europe (mostly Italians) with a wide clinical spectrum of disease symptoms; the sample included 7 subjects who developed acute respiratory distress syndrome requiring extracorporeal membrane oxygenation. The CCR5Δ32 variant was genotyped in all subjects.

Results

The CCR5Δ32 allele was found in one single subject, who developed a very mild form and was not hospitalized.

Conclusions

The CCR5Δ32 allele was not found to be associated with the risk of H1N1pdm09 infection or with a severe disease course.

Keywords: H1N1pdm09 infection, CCR5Δ32, Disease severity

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