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Journal of Clinical Microbiology, September 2004, p. 3950-3957, Vol. 42, No. 9
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.9.3950-3957.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Mutation in a Lordsdale Norovirus Epidemic Strain as a Potential Indicator of Transmission Routes

Kate E. Dingle1,2* Norovirus Infection Control in Oxfordshire Communities Hospitals,{dagger}

Nuffield Department of Clinical Sciences, Oxford University,1 Department of Microbiology, Oxford Radcliffe NHS Trust, John Radcliffe Hospital, Oxford, United Kingdom2

Received 6 April 2004/ Returned for modification 11 May 2004/ Accepted 22 May 2004

An increase in norovirus outbreaks was reported internationally during 2002 and 2003 and was also observed in Oxfordshire (United Kingdom) hospitals. To understand their epidemiological relationships, viruses from 22 outbreaks (15 from one hospital) were subjected to nucleotide sequencing. The 3'-terminal 3,255 nt or complete genomes were determined for 49 viruses. All outbreaks were caused by a genogroup II norovirus related to the Lordsdale virus (GII 4), common in healthcare settings. The norovirus mutation rate was sufficiently high that the 3,255-nucleotide sequences allowed separate and potentially connected outbreaks to be identified, since all outbreaks with identical sequences were temporally or geographically linked. The high mutation rate was further indicated by four mutations and three microheterogeneities in 3,255 nucleotides during 17 days of norovirus shedding by an immunocompromised patient. The data suggested that multiple virus introductions from the community, occasional transmission among wards, and one instance of ongoing environmental contamination had occurred. The accumulation, or lack, of mutations within an outbreak was also used to indicate the predominant transmission route. In an outbreak where person-to-person spread was thought to predominate, six mutations were detected throughout the genome, whereas one mutation was detected when point source infection was suspected. This norovirus epidemic strain differed from its closest previously described relative by 11.4 to 13.6% in the outer P2 domain of the capsid, which also had a single-amino-acid insertion. Alterations to the capsid structure compared to previous noroviruses may explain the increased number of outbreaks during 2002 and 2003.

* Corresponding author. Mailing address: Nuffield Department of Clinical Sciences, Oxford University, John Radcliffe Hospital, Oxford, United Kingdom, OX3 9DU. Phone: 44 1865 220870. Fax: 44 1865 764192. E-mail: kate.dingle{at}ndcls.ox.ac.uk.

{dagger} The contributing members of Norovirus Infection Control in Oxfordshire Communities and Hospitals (NICOCH) are listed in Acknowledgments.

Journal of Clinical Microbiology, September 2004, p. 3950-3957, Vol. 42, No. 9
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.9.3950-3957.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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