Heterozygosity for the F508del Mutation in the Cystic Fibrosis Transmembrane Conductance Regulator Anion Channel Attenuates Influenza Severity | Zendy

Famke Aeffner | Zendy; Basant Abdulrahman | Zendy; Judy M. HickmanDavis | Zendy; Paul M.L. Janssen | Zendy; Amal O. Amer | Zendy; David M. Bedwell | Zendy; Eric J. Sorscher | Zendy; Ian C. Davis | Zendy

Open Access

Heterozygosity for the F508del Mutation in the Cystic Fibrosis Transmembrane Conductance Regulator Anion Channel Attenuates Influenza Severity

Author(s) -

Famke Aeffner,

Basant Abdulrahman,

Judy M. HickmanDavis,

Paul M.L. Janssen,

Amal O. Amer,

David M. Bedwell,

Eric J. Sorscher,

Ian C. Davis

Publication year - 2013

Publication title -

the journal of infectious diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.69

H-Index - 252

eISSN - 1537-6613

pISSN - 0022-1899

DOI - 10.1093/infdis/jit251

Subject(s) - cystic fibrosis transmembrane conductance regulator , cystic fibrosis , mutation , regulator , loss of heterozygosity , heterozygote advantage , compound heterozygosity , ion channel , medicine , transmembrane protein , biology , conductance , cancer research , virology , genetics , chemistry , gene , genotype , allele , physics , receptor , condensed matter physics

Seasonal and pandemic influenza are significant public health concerns. Influenza stimulates respiratory epithelial Cl(-) secretion via the cystic fibrosis transmembrane conductance regulator (CFTR). The purpose of this study was to determine the contribution of this effect to influenza pathogenesis in mice with reduced CFTR activity.

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