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Abstract
In 2010, a large outbreak of rotavirus gastroenteritis occurred in the Alice Springs region of the Northern Territory, Australia. The outbreak occurred 43 months after the introduction of the G1P[8] rotavirus vaccine Rotarix®. Forty-three infants were hospitalized during the outbreak and analysis of fecal samples from each infant revealed a G1P[8] rotavirus strain. The outbreak strain was adapted to cell culture and neutralization assays were performed using VP7 and VP4 neutralizing monoclonal antibodies. The outbreak strain exhibited a distinct neutralization resistance pattern compared to the Rotarix® vaccine strain. Whole genome sequencing of the 2010 outbreak virus strain demonstrated numerous amino acid differences compared to the Rotarix® vaccine strain in the characterized neutralization epitopes of the VP7 and VP4 proteins. Phylogenetic analysis of the outbreak strain revealed a close genetic relationship to global strains, in particular RVA/Human-wt/BEL/BE0098/2009/G1P[8] and RVA/Human-wt/BEL/BE00038/2008/G1P[8] for numerous genes. The 2010 outbreak strain was likely introduced from a globally circulating population of strains rather than evolving from an endemic Australian strain. The outbreak strain possessed antigenic differences in the VP7 and VP4 proteins compared to the Rotarix® vaccine strain. The outbreak was associated with moderate vaccine coverage and possibly low vaccine take in the population.
We gratefully acknowledge Dr Nicole Donker (Enteric Virus Group, Murdoch Childrens Research Institute, Royal Children's Hospital, Melbourne, Australia) for assistance with structural analysis of the VP7 protein and critical review of the manuscript. We thank Timothy Stockwell, Natalie Fedorova and Susmita Shrivastava (The J Craig Venter Institute, Rockville, MD, USA) for assistance with assembly, closure and annotation of viral segment sequences. Carl D Kirkwood is director of Australian Rotavirus Surveillance Program, which is supported by research grants from vaccine manufacturers CSL, GSK and Merck. This work was supported by grants from the National Health and Medical Research Council (NHMRC) of Australia (1031473); Australian Commonwealth Department of Health; GSK Biologicals (Melbourne, Australia); and CSL (Melbourne, Australia). Carl D Kirkwood is supported by a Career Development Award from the NHMRC of Australia (607347). Thomas L Snelling is supported by a NHMRC Frank Fenner Early Career Research Fellowship (1036229) and by a Fiona Stanley Investigator Award. This study was supported by the Victorian Government's Operational Infrastructure Support Program. This project was funded in part with federal funds from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Health and Human Services under contract number HHSN272200900007C.
Supplementary information
Note: Supplementary Information for this article can be found on Emerging Microbes and Infections' website (http://www.nature.com/emi/).