lunes, 16 de marzo de 2015

Innate susceptibility to norovirus infections influenced by FUT2 genotype in a United States pediatric population.

http://www.ncbi.nlm.nih.gov/pubmed/25744498

 2015 Mar 5. pii: civ165. [Epub ahead of print]

Innate susceptibility to norovirus infections influenced by FUT2 genotype in a United States pediatric population.

Abstract

BACKGROUND:

 Norovirus is a leading cause of acute gastroenteritis (AGE). Noroviruses bind to gut histo-blood group antigens (HBGAs), but only 70-80% of individuals have a functional copy of the FUT2 ("secretor") gene required for gut HBGA expression; these individuals are known as "secretors." Susceptibility to some noroviruses depends on FUT2 secretor status, but the population impact of this association is not established.

METHODS:

 From 12/2011 to 11/2012, active AGE surveillance was performed at six geographically diverse US pediatric sites. Cases under five years were recruited from emergency departments and inpatient units; age-matched healthy controls were recruited at well-child visits. Salivary DNA was collected to determine secretor status and genetic ancestry. Stool was tested for norovirus by realtime RT-PCR. Norovirus genotype was then determined by sequencing.

RESULTS:

 Norovirus was detected in 302 (21%) of 1465 AGE cases and 52 (6%) of 826 healthy controls. Norovirus AGE cases were 2.8-fold more likely than norovirus-negative controls to be secretors (p< 0.001) in a logistic regression model adjusted for ancestry, age, site, and health insurance. Secretors comprised all 155 cases and 21 asymptomatic infections with the most prevalent norovirus, GII.4. Control children of Meso-American ancestry were more likely than children of European or African ancestry to be secretors (96% versus 74%, p< 0.001).

CONCLUSIONS:

 FUT2 status is associated with norovirus infection and varies by ancestry. GII.4 norovirus exclusively infected secretors. These findings are important to norovirus vaccine trials and design of agents that may block norovirus-HBGA binding.
© 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:
 
25744498
 
[PubMed - as supplied by publisher]

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