The G428A Nonsense Mutation in FUT2 Provides Strong but Not Absolute Protection against Symptomatic GII.4 Norovirus Infection

被引:110
作者
Carlsson, Beatrice
Kindberg, Elin
Buesa, Javier
Rydell, Gustaf E.
Lidon, Marta Fos
Montava, Rebeca
Abu Mallouh, Reem
Grahn, Ammi
Rodriguez-Diaz, Jesus
Bellido, Juan
Arnedo, Alberto
Larson, Goran
Svensson, Lennart
机构
[1] Division of Molecular Virology, University of Linköping, Linköping
[2] Department of Forensic Genetics and Forensic Toxicology, National Board of Forensic Medicine, Linköping
[3] Department of Microbiology, School of Medicine, University of Valencia, Valencia
[4] Department of Clinical Chemistry and Transfusion Medicine, Sahlgrenska University Hospital, Göteborg
[5] Sección de Epidemiología, Centro de Salud Pública, CIBER-ESP, Castellón
来源
PLOS ONE | 2009年 / 4卷 / 05期
关键词
BLOOD GROUP ANTIGENS; ROUND-STRUCTURED VIRUSES; ACUTE GASTROENTERITIS; UNITED-STATES; P2; DOMAIN; SECRETOR FUT2; OUTBREAKS; SUSCEPTIBILITY; RESISTANCE; BINDING;
D O I
10.1371/journal.pone.0005593
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
In November 2004, 116 individuals in an elderly nursing home in El Grao de Castellon, Spain were symptomatically infected with genogroup II.4 (GII.4) norovirus. The global attack rate was 54.2%. Genotyping of 34 symptomatic individuals regarding the FUT2 gene revealed that one patient was, surprisingly, a non-secretor, hence indicating secretor-independent infection. Lewis genotyping revealed that Lewis-positive and negative individuals were susceptible to symptomatic norovirus infection indicating that Lewis status did not predict susceptibility. Saliva based ELISA assays were used to determine binding of the outbreak virus to saliva samples. Saliva from a secretor-negative individual bound the authentic outbreak GII.4 Valencia/2004/Es virus, but did not in contrast to secretor-positive saliva bind VLP of other strains including the GII.4 Dijon strain. Amino acid comparison of antigenic A and B sites located on the external loops of the P2 domain revealed distinct differences between the Valencia/2004/Es and Dijon strains. All three aa in each antigenic site as well as 10/11 recently identified evolutionary hot spots, were unique in the Valencia/2004/Es strain compared to the Dijon strain. To the best of our knowledge, this is the first example of symptomatic GII.4 norovirus infection of a Le(a+b-) individual homozygous for the G428A nonsense mutation in FUT2. Taken together, our study provides new insights into the host genetic susceptibility to norovirus infections and evolution of the globally dominating GII.4 viruses.
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页数:10
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