tetano
Editor, Senior Moderator
PLoS One. 2015 Sep 17;10(9):e0135983. doi: 10.1371/journal.pone.0135983. eCollection 2015.
[h=1]No Major Host Genetic Risk Factor Contributed to A(H1N1)2009 Influenza Severity.[/h] Garcia-Etxebarria K[SUP]1[/SUP], Bracho MA[SUP]2[/SUP], Gal?n JC[SUP]3[/SUP], Pumarola T[SUP]4[/SUP], Castilla J[SUP]5[/SUP], Ortiz de Lejarazu R[SUP]6[/SUP], Rodr?guez-Dominguez M[SUP]7[/SUP], Quintela I[SUP]8[/SUP], Bonet N[SUP]1[/SUP], Garcia-Garcer? M[SUP]1[/SUP], Dom?nguez A[SUP]9[/SUP], Gonz?lez-Candelas F[SUP]2[/SUP], Calafell F[SUP]1[/SUP]; CIBERESP Cases and Controls in Pandemic Influenza Working Group.
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
PMID: 26379185 [PubMed - in process]
[h=1]No Major Host Genetic Risk Factor Contributed to A(H1N1)2009 Influenza Severity.[/h] Garcia-Etxebarria K[SUP]1[/SUP], Bracho MA[SUP]2[/SUP], Gal?n JC[SUP]3[/SUP], Pumarola T[SUP]4[/SUP], Castilla J[SUP]5[/SUP], Ortiz de Lejarazu R[SUP]6[/SUP], Rodr?guez-Dominguez M[SUP]7[/SUP], Quintela I[SUP]8[/SUP], Bonet N[SUP]1[/SUP], Garcia-Garcer? M[SUP]1[/SUP], Dom?nguez A[SUP]9[/SUP], Gonz?lez-Candelas F[SUP]2[/SUP], Calafell F[SUP]1[/SUP]; CIBERESP Cases and Controls in Pandemic Influenza Working Group.
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
PMID: 26379185 [PubMed - in process]