tetano
Editor, Senior Moderator
J Infect Dis. 2015 Apr 22. pii: jiv246. [Epub ahead of print]
[h=1]The identification of TMPRSS2 as the susceptible gene for severe illness of 2009 pandemic A(H1N1) influenza and infection of A(H7N9) influenza.[/h] Cheng Z[SUP]1[/SUP], Zhou J[SUP]2[/SUP], To KK[SUP]3[/SUP], Chu H[SUP]2[/SUP], Li C[SUP]1[/SUP], Wang D[SUP]1[/SUP], Yang D[SUP]1[/SUP], Zheng S[SUP]4[/SUP], Hao K[SUP]5[/SUP], Boss? Y[SUP]6[/SUP], Obeidat M[SUP]7[/SUP], Brandsma CA[SUP]8[/SUP], Song YQ[SUP]9[/SUP], Chen Y[SUP]4[/SUP], Zheng BJ[SUP]2[/SUP], Li L[SUP]4[/SUP], Yuen KY[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The genetic predisposition to severe A(H1N1)pdm09 influenza was evaluated in 409 patients including 162 severe cases and 247 mild controls. We prioritized candidate variants based on the result of a pilot GWAS and a lung eQTL dataset. The GG genotype of rs2070788, a higher-expression variant of TMPRSS2, was a risk variant (OR 2.11, 95% CI 1.18∼3.77, P=0.0113) to severe A(H1N1)pdm09 influenza. A potentially functional SNP, rs383510, accommodated in a putative regulatory region was identified to tag rs2070788. Luciferase assay results showed the putative regulatory region was a functional element, in which rs383510 regulated TMPRSS2 expression in a genotype-specific manner. Notably, rs2070788 and rs383510 were significantly associated with the susceptibility to A(H7N9) influenza in 102 A(H7N9) patients and 106 healthy controls. Therefore, we demonstrate that genetic variants with higher TMPRSS2 expression confer higher risk to severe A(H1N1)pdm09 influenza. The same variants also increase the susceptibility to human A(H7N9) influenza.
? The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
PMID: 25904605 [PubMed - as supplied by publisher]
[h=1]The identification of TMPRSS2 as the susceptible gene for severe illness of 2009 pandemic A(H1N1) influenza and infection of A(H7N9) influenza.[/h] Cheng Z[SUP]1[/SUP], Zhou J[SUP]2[/SUP], To KK[SUP]3[/SUP], Chu H[SUP]2[/SUP], Li C[SUP]1[/SUP], Wang D[SUP]1[/SUP], Yang D[SUP]1[/SUP], Zheng S[SUP]4[/SUP], Hao K[SUP]5[/SUP], Boss? Y[SUP]6[/SUP], Obeidat M[SUP]7[/SUP], Brandsma CA[SUP]8[/SUP], Song YQ[SUP]9[/SUP], Chen Y[SUP]4[/SUP], Zheng BJ[SUP]2[/SUP], Li L[SUP]4[/SUP], Yuen KY[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The genetic predisposition to severe A(H1N1)pdm09 influenza was evaluated in 409 patients including 162 severe cases and 247 mild controls. We prioritized candidate variants based on the result of a pilot GWAS and a lung eQTL dataset. The GG genotype of rs2070788, a higher-expression variant of TMPRSS2, was a risk variant (OR 2.11, 95% CI 1.18∼3.77, P=0.0113) to severe A(H1N1)pdm09 influenza. A potentially functional SNP, rs383510, accommodated in a putative regulatory region was identified to tag rs2070788. Luciferase assay results showed the putative regulatory region was a functional element, in which rs383510 regulated TMPRSS2 expression in a genotype-specific manner. Notably, rs2070788 and rs383510 were significantly associated with the susceptibility to A(H7N9) influenza in 102 A(H7N9) patients and 106 healthy controls. Therefore, we demonstrate that genetic variants with higher TMPRSS2 expression confer higher risk to severe A(H1N1)pdm09 influenza. The same variants also increase the susceptibility to human A(H7N9) influenza.
? The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
PMID: 25904605 [PubMed - as supplied by publisher]