This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cannon, J. L.
Right arrow Articles by Vinjé, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cannon, J. L.
Right arrow Articles by Vinjé, J.

 Previous Article  |  Next Article 

Journal of Virology, June 2009, p. 5363-5374, Vol. 83, No. 11
0022-538X/09/$08.00+0     doi:10.1128/JVI.02518-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Herd Immunity to GII.4 Noroviruses Is Supported by Outbreak Patient Sera{triangledown}

Jennifer L. Cannon,1,2,3* Lisa C. Lindesmith,4 Eric F. Donaldson,4 Lauryn Saxe,1 Ralph S. Baric,4 and Jan Vinjé1

Centers for Disease Control and Prevention, Atlanta, Georgia 30333,1 Department of Environmental Science and Engineering, University of North Carolina—Chapel Hill, Chapel Hill, North Carolina 27599,2 Atlanta Research and Education Foundation, Decatur, Georgia 30033,3 Department of Epidemiology, University of North Carolina—Chapel Hill, Chapel Hill, North Carolina 275994

Received 8 December 2008/ Accepted 10 March 2009

Noroviruses (NoVs) of genogroup II, cluster 4 (GII.4), are the most common cause of outbreaks of acute gastroenteritis worldwide. During the past 13 years, GII.4 NoVs caused four seasons of widespread activity globally, each associated with the emergence of a new strain. In this report, we characterized the most recent epidemic strain, GII.4-2006 Minerva, by comparing virus-like particle (VLP) antigenic relationships and histo-blood group antigen (HBGA) binding profiles with strains isolated earlier. We also investigated the seroprevalence and specificity of GII.4 antibody in the years prior to, during, and following the GII.4 pandemic of 1995 and 1996 using a large collection of acute- and convalescent-phase serum pairs (n = 298) collected from 34 outbreaks. In a surrogate neutralization assay, we measured the blockade of HBGA binding using a panel of GII.4 VLPs representing strains isolated in 1987, 1997, 2002, and 2006 and a GII.3 VLP representing a strain isolated in the mid-1990s. Serum titers required for 50% HBGA blockade were compared between populations. In general, blockade of GII.4 VLP-HBGA binding was greater with convalescent-phase outbreak sera collected near the time of origin of the VLP strain. Heterotypic genotypes did not contribute to herd immunity against GII.4 NoVs based on their inability to block GII.4 VLP binding to HBGA. However, previous exposure to GII.4 NoV followed by infection by GII.3 NoV appeared to evoke an immune response to GII.4 NoV. These results support the hypothesis that herd immunity is a driving force for GII.4 evolution in the U.S. population. The data also suggest that complex patterns of cross-protection may exist across NoV genotypes in humans.

* Corresponding author. Present address: University of Georgia Center for Food Safety, 1109 Experiment St., Griffin, GA 30223. Phone: (770) 467-6094. Fax: (770) 229-3216. E-mail: jcannon{at}uga.edu

{triangledown} Published ahead of print on 18 March 2009.

Journal of Virology, June 2009, p. 5363-5374, Vol. 83, No. 11
0022-538X/09/$08.00+0     doi:10.1128/JVI.02518-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»