No Major Host Genetic Risk Factor Contributed to A(H1N1)2009 Influenza Severity
Garcia-Etxebarria, Koldo (Institut de Biologia Evolutiva (UPF-CSIC) (Barcelona))
Bracho, Maria Alma (Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública)
Galán, Juan Carlos (Instituto Ramón y Cajal de Investigación Sanitaria (Madrid))
Pumarola Suñé, Tomàs (Hospital Universitari Vall d'Hebron)
Castilla, Jesus (Instituto de Investigación Sanitaria de Navarra)
Ortiz de Lejarazu, Raúl (Hospital Clínico Universitario de Valladolid)
Rodríguez-Dominguez, Mario (Red Española de Investigación en Patología Infecciosa)
Quintela, Inés (Universidade de Santiago de Compostela)
Bonet, Núria (Institut de Biologia Evolutiva (UPF-CSIC) (Barcelona))
Garcia-Garcerà, Marc (Institut de Biologia Evolutiva (UPF-CSIC) (Barcelona))
Domínguez, Ángela (Universitat de Barcelona. Departament de Salut Pública)
González-Candelas, Fernando (Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública)
Calafell, Francesc (Institut de Biologia Evolutiva (UPF-CSIC) (Barcelona))
Universitat Autònoma de Barcelona

Data:	2015
Resum:	While most patients affected by the influenza A(H1N1) pandemic experienced mild symptoms, a small fraction required hospitalization, often without concomitant factors that could explain such a severe course. We hypothesize that host genetic factors could contribute to aggravate the disease. To test this hypothesis, we compared the allele frequencies of 547,296 genome-wide single nucleotide polymorphisms (SNPs) between 49 severe and 107 mild confirmed influenza A cases, as well as against a general population sample of 549 individuals. When comparing severe vs. mild influenza A cases, only one SNP was close to the conventional p = 5×10 −8. This SNP, rs28454025, sits in an intron of the GSK233 gene, which is involved in a neural development, but seems not to have any connections with immunological or inflammatory functions. Indirectly, a previous association reported with CD55 was replicated. Although sample sizes are low, we show that the statistical power in our design was sufficient to detect highly-penetrant, quasi-Mendelian genetic factors. Hence, and assuming that rs28454025 is likely to be a false positive, no major genetic factor was detected that could explain poor influenza A course.
Ajuts:	Instituto de Salud Carlos III GR09/0032
Drets:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Llengua:	Anglès
Document:	Article ; recerca ; Versió publicada
Publicat a:	PloS one, Vol. 10 (september 2015) , ISSN 1932-6203

DOI: 10.1371/journal.pone.0135983
PMID: 26379185

10 p, 1.5 MB

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