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Chapter 49 : Human Caliciviruses

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Human Caliciviruses, Page 1 of 2

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Abstract:

Norwalk virus (NV) was first recognized from an outbreak of epidemic gastroenteritis in an elementary school in Norwalk, Ohio in 1968, in which 50% of the students and teachers became ill and secondary cases occurred in 32% of family contacts (1). Subsequently, NV was visualized using immune electron microscopy (IEM) and described as a 27-nm filterable agent (2). This provided definitive proof that viruses cause diarrhea, an idea initially proposed during the 1940s and 1950s when a filterable infectious agent (although not propagated in cell culture) was passaged serially in volunteers. The first clear description of the basic virological, clinical, and immunological responses to nonbacterial infections came from studies in volunteers administered a bacteria-free fecal filtrate of NV (3). The history of these early investigations leading to visualization of the agent by IEM provides an excellent example of how major scientific advances often require and parallel new technological opportunities (4). The subsequent application of IEM to other diarrheal stool samples ultimately led to the discovery of other viral agents of gastroenteritis and hepatitis A virus (see Chapters 4, 25, 34, and 48). The later cloning and expression of the NV genome resulted in the development of new assays and reagents that permit large-scale epidemiologic studies.

Citation: Atmar R, Estes M. 2017. Human Caliciviruses, p 1189-1208. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch49
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Figures

Image of FIGURE 1
FIGURE 1

Negative-stain electron micrographs of (A) an NoV (previously called small round-structured virus, or SRSV) from the stool of a volunteer given NoV/NV/8fIIa; (B) an SaV with the classical calicivirus morphologic features including distinct cuplike indentations in the surface of the particles, taken from the stool of a child and containing SaV/Sapporo; (C) 38 nm rNV particles produced and purified from insect cells infected with a baculovirus recombinant that expresses the NV ORF2; and (D) 19-nm particles produced and purified from insect cells infected with a baculovirus recombinant that expresses NV ORF2. Bar, 50 nm. Panel D adapted from White et al. (33) and courtesy of Dr. L. White.

Citation: Atmar R, Estes M. 2017. Human Caliciviruses, p 1189-1208. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch49
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Image of FIGURE 2
FIGURE 2

(a) Surface representation of the three-dimensional surface structure of rNV particles viewed along the icosahedral 3-fold axis. This structure was determined by image processing of the rNV particles shown in Figure 1c . The rNV particles have a distinct architecture and they exhibit T = 3 icosahedral symmetry; the 2-fold, 3-fold, and 5-fold axes of symmetry are shown. Cuplike depressions are evident at the 3-fold and 5-fold axes. The capsid structure is made up of 90 archlike dimers of a single protein that form two types of capsomers; A/B capsomeres (n=60) surround the 3- and 5-fold axes of symmetry and C/C capsomers (n=30) are located at the 2-fold axes of symmetry. (b) Summary of the properties of the single protein that makes up the NV capsid structure. A linear schematic of the three domains (c, conserved; v, variable; lc, less conserved) in the single capsid protein and a region predicted to fold into an eight-stranded antiparallel beta-barrel is shown. (c) X-ray crystallographic structure of rNV capsid at 3.4 Å resolution, as viewed along icosahedral 2-fold axis. Only backbone atoms of the 180 subunits are depicted, and the structure is depth-cued, with deeper blue at lower radii and lighter blue at higher radii. (d) Ribbon presentation of the C subunit of rNV capsid protein. N-terminal arm, S domain, P1 and P2 subdomains are colored in green, yellow, red, and blue, respectively. N- and C-termini of the capsid protein are indicated. The C-terminus faces a hollow, the N-terminus faces the interior of the capsid, and the P2 subdomain faces the exterior of the capsid. Figures a, c, and d kindly provided by B.V.V. Prasad; modified from Prasad et al. (27, 28), with permission.

Citation: Atmar R, Estes M. 2017. Human Caliciviruses, p 1189-1208. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch49
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Image of FIGURE 3
FIGURE 3

Schematic of the genomic organization of two human genogroup I and II NoVs, the murine genogroup V NoV and a human genogroup II SaV. The NoVs have three predicted ORFs that include ( ) ORF1, a polyprotein that contains the nonstructural proteins NS1-NS7; ( ) ORF2, the major capsid protein (VP1); and ( ) ORF3, a minor capsid protein (VP2). For SaVs, ORF1 is longer and contains the major capsid protein, VP1 (see text for details). Nucleotide numbers denoting ORFs are indicated for each of the viruses. Molecular weights of each of the viral proteins are also indicated. Among the NoVs, NS1/NS2 forms a single protein, and for the SaV strain indicated, NS6/NS7 forms a single protein. This information is compiled from GenBank sequences M87661 (NV), AF145896 (Camberwell), AY228235 (Murine), and AY237420 (Mc10) and selected references ( ).

Citation: Atmar R, Estes M. 2017. Human Caliciviruses, p 1189-1208. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch49
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Image of FIGURE 4
FIGURE 4

Jejunal tissue from biopsies of a volunteer prior to challenge (A) and after challenge (B) with Norwalk virus. The villi are broadened and flattened during Norwalk virus gastroenteritis illness. (H&E, x90.) From Agus et al. ( ), with permission.

Citation: Atmar R, Estes M. 2017. Human Caliciviruses, p 1189-1208. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch49
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Image of FIGURE 5
FIGURE 5

Clinical course of two volunteers who became ill after challenge with 8fIIa NV inoculum (at 0 h). Both volunteers were considered to have severe disease. Volunteer 503 was a 29-year-old man and volunteer 516 was a 23-year-old woman ( ).

Citation: Atmar R, Estes M. 2017. Human Caliciviruses, p 1189-1208. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch49
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