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    Phylodynamic reconstruction reveals norovirus GII.4 epidemic expansions and their molecular determinants

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    Phylodynamic reconstruction ...
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    Genre
    Journal Article
    Date
    2010-01-01
    Author
    Siebenga, JJ
    Lemey, P
    Pond, SLK
    Rambaut, A
    Vennema, H
    Koopmans, M
    Subject
    Amino Acid Substitution
    Bayes Theorem
    Caliciviridae Infections
    Capsid Proteins
    Dimerization
    Disease Outbreaks
    Epistasis, Genetic
    Evolution, Molecular
    Gastroenteritis
    Models, Genetic
    Norovirus
    Nucleic Acid Conformation
    Open Reading Frames
    Phylogeny
    RNA, Viral
    Virus Replication
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    Permanent link to this record
    http://hdl.handle.net/20.500.12613/5552
    
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    DOI
    10.1371/journal.ppat.1000884
    Abstract
    Noroviruses are the most common cause of viral gastroenteritis. An increase in the number of globally reported norovirus outbreaks was seen the past decade, especially for outbreaks caused by successive genogroup II genotype 4 (GII.4) variants. Whether this observed increase was due to an upswing in the number of infections, or to a surveillance artifact caused by heightened awareness and concomitant improved reporting, remained unclear. Therefore, we set out to study the population structure and changes thereof of GII.4 strains detected through systematic outbreak surveillance since the early 1990s. We collected 1383 partial polymerase and 194 full capsid GII.4 sequences. A Bayesian MCMC coalescent analysis revealed an increase in the number of GII.4 infections during the last decade. The GII.4 strains included in our analyses evolved at a rate of 4.3-9.0×10-3 mutations per site per year, and share a most recent common ancestor in the early 1980s. Determinants of adaptation in the capsid protein were studied using different maximum likelihood approaches to identify sites subject to diversifying or directional selection and sites that co-evolved. While a number of the computationally determined adaptively evolving sites were on the surface of the capsid and possible subject to immune selection, we also detected sites that were subject to constrained or compensatory evolution due to secondary RNA structures, relevant in virus-replication. We highlight codons that may prove useful in identifying emerging novel variants, and, using these, indicate that the novel 2008 variant is more likely to cause a future epidemic than the 2007 variant. While norovirus infections are generally mild and self-limiting, more severe outcomes of infection frequently occur in elderly and immunocompromized people, and no treatment is available. The observed pattern of continually emerging novel variants of GII.4, causing elevated numbers of infections, is therefore a cause for concern. © 2010 Siebenga et al.
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    Public Library of Science (PLoS)
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    PLoS Pathogens
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    http://dx.doi.org/10.34944/dspace/5534
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