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Review
. 2003 Sep;77(17):9109-15.
doi: 10.1128/jvi.77.17.9109-9115.2003.

Reovirus receptors and pathogenesis

J Craig Forrest  1 , Terence S Dermody
Affiliations
Review

Reovirus receptors and pathogenesis

J Craig Forrest et al. J Virol. 2003 Sep.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Crystal structure of reovirus attachment protein σ1. The crystal structure of T3D σ1 includes residues 245 to 455 (14). The three monomers of the σ1 trimer are shown in red, orange, and blue. Each monomer consists of a C-terminal head domain formed by a compact β-barrel and an N-terminal fibrous tail that contains three β-spiral repeats. Based on analysis of patterns in aligned σ1 sequences, the β-spiral likely begins at residue 167 of T3D σ1 and comprises eight repeats. The N-terminal five repeats, which are not included in the crystal structure, are shown in gray. The spiral has been extended using translated and rotated σ1 repeats to generate a model that depicts the approximate dimensions of the molecule. Amino acids Asn198, Arg202, and Pro204 have been implicated in the interaction of T3D σ1 with sialic acid (13). The approximate location of these residues in the model (shown in ball-and-stick representation on the right) suggests that they form a binding site for sialic acid. Residues 1 to 167 are not shown; these residues are predicted to form a triple α-helical coiled coil structure (6, 25, 27, 40). This figure was prepared by Thilo Stehle (Harvard University) (published with permission) with the program RIBBONS (10).
FIG. 2.
FIG. 2.
(A to D) Liver histopathology in mice following infection with T3SA− and T3SA+. ND4 Swiss Webster mice (2 to 3 days old) were inoculated perorally with phosphate-buffered saline (A) or 2.5 × 103 PFU of either T3SA− (B) or T3SA+ (C and D). At 8 days postinoculation, liver tissue was harvested, embedded in paraffin, thin sectioned, and stained with hematoxylin and eosin. Magnification, ×100 (C) or ×400 (A, B, and D). (E to H) Immunohistochemical localization of reovirus antigen in bile duct epithelial cells. ND4 Swiss Webster mice (2 to 3 days old) were inoculated perorally with 2.5 × 103 PFU of either T3SA− (E and F) or T3SA+ (G and H). At 6 days postinoculation, liver tissue was harvested, embedded in paraffin, thin sectioned, and stained for reovirus antigen using rabbit anti-reovirus serum and horseradish peroxidase. Dark-brown staining indicates the presence of reovirus antigen. Magnification, ×400. Representative sections from two separate animals are shown. Modified from Barton et al. (5) with permission from the publisher.
FIG. 3.
FIG. 3.
Model of reovirus-induced apoptosis. Reovirus infection is initiated by attachment of the virus to carbohydrate coreceptors and JAM1. For T3 reoviruses, the carbohydrate bound is sialic acid (SA). After attachment to cellular receptors, reovirus enters cells by receptor-mediated endocytosis. Within an endocytic compartment, the viral outer capsid is removed to generate infectious subvirion particles (ISVPs). During virion-to-ISVP conversion, σ3 is degraded and lost from virions, σ1 undergoes a conformational change, and μ1 is cleaved to form particle-associated fragments δ and φ. Removal of σ3 exposes hydrophobic domains in μ1 that facilitate interactions of ISVPs with endosomal membranes, leading to delivery of core particles into the cytoplasm and concomitant activation of the viral transcriptase. Viral attachment and disassembly must occur within the same cellular compartment to activate NF-κB. Activation of NF-κB also might be achieved by μ1-mediated membrane penetration acting in synergy with viral receptor engagement. Once activated, NF-κB translocates to the nucleus, where it induces the expression of proapoptotic genes.
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