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Chapter 12 : Genome Diversity and Host Interaction of Noroviruses

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Abstract:

The epidemic and sporadic forms of gastroenteritis are common causes of morbidity in developed countries and of morbidity and mortality in developing countries. Although the current review focuses on viral causes of acute gastroenteritis, it can also be caused by bacteria or parasites. Recent studies employing molecular and antigenic methods for detection of enteric viruses showed that the majority of acute viral gastroenteritis cases worldwide are caused by noroviruses (NVs). The molecular cloning and genomic characterization of other viral strains has greatly facilitated our understanding of the genetic structure and classification of NVs. The RNA genome is organized into three open reading frames (ORFs). Several studies were undertaken in recent years to improve understanding of the mechanisms and biological advantages of genotype GII.4 epidemic strains. A study showed that GII.4 NVs evolve stepwise by highly significant preferential accumulation and fixation of nucleotide and amino acid mutations in the protruding part of the capsid protein. Another study showed that the NV capsid protein accumulates mutations more rapidly in healthy immunocompetent individuals than in immunocompromised individuals. In this study, 66 P2 sequences from viruses isolated during outbreaks occurring between 1997 and 2006 in the United Kingdom showed diversity of up to 20%. Further high-resolution structural studies are necessary to determine the role of the P2 subdomain in host interactions and to understand its possible role in NV strain diversity.

Citation: Schreier E. 2012. Genome Diversity and Host Interaction of Noroviruses, p 191-213. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch12

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Figures

Image of FIGURE 1
FIGURE 1

NV particles from a stool filtrate of a patient with acute gastroenteritis. The particles were negatively stained with uranyl acetate and visualized by electron microscopy. They are about 35 nm in diameter. Bar, 100 nm. Courtesy of the Robert Koch Institute, Berlin, Germany.

Citation: Schreier E. 2012. Genome Diversity and Host Interaction of Noroviruses, p 191-213. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch12
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Image of FIGURE 2
FIGURE 2

Schematic diagram showing the organization of the NV genome and putative cleavage products of the ORF1 polyprotein. Values represent the molecular mass of the predicted protein products (in kilodaltons). The nucleotide position (GenBank accession number M87661) is indicated along the top.

Citation: Schreier E. 2012. Genome Diversity and Host Interaction of Noroviruses, p 191-213. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch12
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Image of FIGURE 3
FIGURE 3

Capsid structure of the NV VLP solved by cryoelectron microscopic reconstruction (top, surface representation; bottom, cross section) and by X-ray crystallography. The VLP contains 90 dimers of capsid protein assembled in T=3 icosahedral symmetry (left, ribbon diagram). Each monomeric capsid protein (right, ribbon diagram) is divided into an N-terminal arm region (green) facing the interior of the VLP, a shell (S) domain (yellow) that forms the continuous surface of the VLP, and a protruding (P) domain that constitutes the arch at the surface of the VLP. The P domain is further divided into subdomains P1 and P2 (red and blue, respectively). The P2 subdomain is implicated in virus-host interactions. Reprinted from with permission.

Citation: Schreier E. 2012. Genome Diversity and Host Interaction of Noroviruses, p 191-213. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch12
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Image of FIGURE 4
FIGURE 4

Phylogenetic relationships within the genus Full-length capsid nucleotide sequences were used for the phylogenetic analysis and included a representative strain from each genotype of genogroups GI to GV. Phylogenetic analysis (neighbor-joining method) was performed with BioEdit (version 7.09, copyright T. A. Hall), which includes the Phylogeny Interference Package (PHYLIP) from J. Felsenstein. Evolutionary distances were calculated by the Kimura two-parameter method ( ). The scale bar represents the phylogenetic distances expressed as units of expected nucleotide substitutions per site. GenBank accession numbers for the genotypes in the analysis were as follows: GI.1 (M87661), GI.2 (L07418), GI.3 (U04469), GI.4 (AB042808), GI.5 (AJ277614), GI.6 (AF093797), GI.7 (AJ277609), GI.8 (AF538679), GII.1 (U07611), GII.2 (AY134748), GII.3 (U22498), GII.4 (X86557), GII.5 (AJ277607), GII.6 (AJ277620), GII.7 (AJ277608), GII.8 (AF195848), GII.9 (AY038599),GII.10 (AF427118), GII.11 (AB074893), GII.12 (AJ277618), GII.13 (AY113106), GII.14 (AY130761), GII.15 (AY130762), GII.16 (AY502010), GII.17 (AY502009), GII.18 (AY823304), GII.19 (AY823306), GIII.1 (AJ011099), GIII.2 (AF320625), GIV.1 (AF195847), GIV.2 (EF450827), and GV (AY228235).

Citation: Schreier E. 2012. Genome Diversity and Host Interaction of Noroviruses, p 191-213. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch12
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Image of FIGURE 5
FIGURE 5

Distribution of major NV genotypes in Germany between January 2001 and December 2008. Genotyping was done based on partial RdRp sequence data (M. Hoehne and E. Schreier, Robert Koch Institute, Berlin, Germany, unpublished data). The numbers of reported NV cases in Germany are as follows: 9,292 (2001), 51,619 (2002), 41,755 (2003), 64,794 (2004), 62,773 (2005), 75,865 (2006), 201,227 (2007), and 212,692 (2008) (see ://www3.rki.de/SurvStat).

Citation: Schreier E. 2012. Genome Diversity and Host Interaction of Noroviruses, p 191-213. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch12
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Image of FIGURE 6
FIGURE 6

Electron micrograph of baculovirus-expressed NV capsid protein (VLPs) negatively stained with uranyl acetate. Bar, 100 nm. M. Hoehne, M. Laue, and E. Schreier, Robert Koch Institute, Berlin, Germany, unpublished data.)

Citation: Schreier E. 2012. Genome Diversity and Host Interaction of Noroviruses, p 191-213. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch12
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Tables

Generic image for table
TABLE 1

Taxonomic structure of the

Citation: Schreier E. 2012. Genome Diversity and Host Interaction of Noroviruses, p 191-213. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch12
Generic image for table
TABLE 2

Distribution of norovirus genogroups and genotypes across the various human and animal species

Citation: Schreier E. 2012. Genome Diversity and Host Interaction of Noroviruses, p 191-213. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch12

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