Amino acid changes associated with neurovirulence in the HN or SH gene.

<p>Amino acid changes associated with neurovirulence in the HN or SH gene.</p

Alignment of the inferred aa sequences of the SH gene.

<p>The potential neurovirulence sites are marked in boxes. Period (.) denotes identity with the majority sequence; (-) denotes areas that were not determined; (*) represents Genotype-strain ID.</p

Alignment of the inferred partial aa sequences of the HN gene.

<p>The potential glycosylation sites are shown in shadow and the potential neurovirulence sites are marked in boxes. Period (.) denotes identity with the uppermost sequence; (-) denotes areas that were not determined; (*) represents Genotype-strain ID.</p

Patients and specimens in the study.

<p>Note: OF, Oral fluid; CSF, cerebrospinal fluid; TS, throat swab; TCF, tissue culture fluid; P, parotitis; N, neurological complications; NK: not known; MMR, measles-mumps-rubella vaccine; UK, United Kingdom.</p>*<p>Dominican Republic linked re-infection case in Sweden, childhood infected (Dr. Kari Johansen, Swedish Institute for Infectious Disease Control).</p

Amino acid changes in the hypervariable P2 domain associated with the Sydney2012 strain.

<p>Three-dimensional model of the GII-4 norovirus P domain <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0088978#pone.0088978-Cao1" target="_blank">[6]</a> showing key amino acid positions on the surface of the capsid protein (grey/red). Also indicated are site A (yellow) and site B (blue) (positions 296–298 and 393–395, respectively) <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0088978#pone.0088978-Allen1" target="_blank">[11]</a>. Details of amino acid changes are shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0088978#pone-0088978-t003" target="_blank">Table 3</a>.</p

Regression model results for outbreaks and norovirus strain types in England, May 2012 to June 2013.

<p>Regression model results for outbreaks and norovirus strain types in England, May 2012 to June 2013.</p

Predicted number of HNORS laboratory confirmed outbreaks associated with the Sydney2012 strain by month (May 2012–June 2013) in England.

<p>Grey bars (baseline) include all other strain types, which varies according to winter and summer as norovirus is a seasonal pathogen. Red bars indicate predicted number of HNORS outbreaks associated with Sydney2012. The black line shows the number of observed laboratory confirmed HNORS outbreaks.</p

Detection of NewOrleans2009 and Sydney2012 strains associated with outbreaks (by week) in England during the 2012/13 norovirus season.

<p>Blue bars indicate outbreaks associated with NewOrleans2009. Red bars indicate outbreaks associated with Sydney2012. This figure shows data for 328 norovirus-confirmed outbreaks where GII-4 strains were associated with the outbreak, P2 domain strain typing data could be generated, and a date of outbreak was supplied.</p

Characteristics of mutations at amino acid positions in the P2 domain associated with the Sydney2012.

<p>Amino acid positions 294, 310, 359, 368, 373 and 396 were found to be associated with the Sydney2012 strain, compared with the NewOrleans2009 strain. The characteristics of the amino acid changes at these sites are shown.</p

Distribution of norovirus strains (by genotype) in England during the 2012/13 season.

<p>(##) Per cent of all norovirus-confirmed outbreaks (<i>n</i> = 592).</p