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
Google Scholar
Right arrow Articles by Liu, G.
Right arrow Articles by Karst, S. M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liu, G.
Right arrow Articles by Karst, S. M.

 Previous Article  |  Next Article 

Journal of Virology, July 2009, p. 6963-6968, Vol. 83, No. 13
0022-538X/09/$08.00+0     doi:10.1128/JVI.00284-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Primary High-Dose Murine Norovirus 1 Infection Fails To Protect from Secondary Challenge with Homologous Virus{triangledown}

Guangliang Liu, Shannon M. Kahan, Yali Jia, and Stephanie M. Karst*

Center for Molecular and Tumor Virology, Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932

Received 9 February 2009/ Accepted 19 April 2009

Human noroviruses in the Caliciviridae family are the major cause of nonbacterial epidemic gastroenteritis worldwide. Primary human norovirus infection does not elicit lasting protective immunity, a fact that could greatly affect the efficacy of vaccination strategies. Little is known regarding the pathogenesis of human noroviruses or the immune responses that control them because there has previously been no small-animal model or cell culture system of infection. Using the only available small-animal model of norovirus infection, we found that primary high-dose murine norovirus 1 (MNV-1) infection fails to afford protection against a rechallenge with a homologous virus. Thus, MNV-1 represents a valuable model with which to dissect the pathophysiological basis for the lack of lasting protection against human norovirus infection. Interestingly, the magnitude of protection afforded by a primary MNV-1 infection inversely correlates with the inoculum dose. Future studies will elucidate the mechanisms by which noroviruses avoid the induction of protective immunity and the role played by the inoculum dose in this process, ultimately translating this knowledge into successful vaccination approaches.


* Corresponding author. Mailing address: Center for Molecular and Tumor Virology, Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130. Phone: (318) 675-8122. Fax: (318) 675-5764. E-mail: skarst{at}lsuhsc.edu

{triangledown} Published ahead of print on 29 April 2009.


Journal of Virology, July 2009, p. 6963-6968, Vol. 83, No. 13
0022-538X/09/$08.00+0     doi:10.1128/JVI.00284-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.