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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bridger, J. C.
Right arrow Articles by Desselberger, U.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bridger, J. C.
Right arrow Articles by Desselberger, U.

 Previous Article  |  Next Article 

J Virol, August 1998, p. 6929-6931, Vol. 72, No. 8
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Viral Determinants of Rotavirus Pathogenicity in Pigs: Evidence that the Fourth Gene of a Porcine Rotavirus Confers Diarrhea in the Homologous Host

Janice C. Bridger,1,* Gabriele I. Tauscher,2 and Ulrich Desselberger2

Department of Pathology and Infectious Diseases, The Royal Veterinary College, University of London, London NW1 0TU,1 and Clinical Microbiology and Public Health Laboratory and Division of Virology, Department of Pathology, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 2QW,2 United Kingdom

Received 26 January 1998/Accepted 4 May 1998

A porcine rotavirus (prv) monoreassortant, S-F4, which carries RNA segment 4 of the pig-pathogenic variant prv 4F in the genetic background of the pig-apathogenic variant prv 4S (G. I. Tauscher and U. Desselberger, J. Virol. 71:853-857, 1997), was found to be pathogenic in gnotobiotic piglets. This indicates that RNA segment 4 of the pig-pathogenic variant prv 4F is a major determinant of pathogenicity in its homologous host.

* Corresponding author. Mailing address: Department of Pathology & Infectious Diseases, The Royal Veterinary College, University of London, London NW1 0TU, United Kingdom. Phone: 44-171-468 5221. Fax: 44-171-468 5306. E-mail: jbridger{at}rvc.ac.uk.

J Virol, August 1998, p. 6929-6931, Vol. 72, No. 8
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • McNeal, M. M., Sestak, K., Choi, A. H.-C., Basu, M., Cole, M. J., Aye, P. P., Bohm, R. P., Ward, R. L. (2005). Development of a Rotavirus-Shedding Model in Rhesus Macaques, Using a Homologous Wild-Type Rotavirus of a New P Genotype. J. Virol. 79: 944-954 [Abstract] [Full Text]  
  • Mossel, E. C., Ramig, R. F. (2002). Rotavirus Genome Segment 7 (NSP3) Is a Determinant of Extraintestinal Spread in the Neonatal Mouse. J. Virol. 76: 6502-6509 [Abstract] [Full Text]  
  • Ciarlet, M., Ludert, J. E., Iturriza-Gomara, M., Liprandi, F., Gray, J. J., Desselberger, U., Estes, M. K. (2002). Initial Interaction of Rotavirus Strains with N-Acetylneuraminic (Sialic) Acid Residues on the Cell Surface Correlates with VP4 Genotype, Not Species of Origin. J. Virol. 76: 4087-4095 [Abstract] [Full Text]  
  • Ciarlet, M, Estes, M. (1999). Human and most animal rotavirus strains do not require the presence of sialic acid on the cell surface for efficient infectivity. J. Gen. Virol. 80: 943-948 [Abstract]  


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