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Color Plates

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Figures

Image of Color Plate 1 (chapter 1).

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Color Plate 1 (chapter 1).

Schematic structure of particles of members of the order E, envelope protein; GP and gp, glycoprotein; M, membrane protein; N, nucleoprotein; S, spike glycoprotein. The HEs of some group 2 coronaviruses and some toroviruses are not illustrated. The stoichiometry of the virion components is shown arbitrarily. Adapted from reference 44a.

Citation: Perlman S, Gallagher T, Snijder E. 2008. Color Plates, In Nidoviruses. ASM Press, Washington, DC.
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Image of Color Plate 2 (chapter 1).

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Color Plate 2 (chapter 1).

Models for nidovirus replication and transcription using hypothetical viruses that produce four subgenomic mRNAs. Plus-strand RNA is depicted in red, and minus-strand RNA is depicted in blue. In the case of coronavi-ruses and arteriviruses, discontinuous extension during minus-strand RNA synthesis is proposed as the mechanism to produce subgenome-length minus-strand templates. The RTC is proposed to be attenuated at one of the body TRSs in the 3’-proximal part of the genome, after which the nascent minus strand would be extended with the antileader sequence by a process of discontinuous extension. The completed subgenome-length minus strands would serve as templates for mRNA synthesis. In the case of roniviruses and all but the largest subgenome-length mRNA of toroviruses, conserved attenuation sequences, found upstream of each of the genes in the 3’-proximal part of the genome, direct the termination of nascent minus-strand synthesis. The attenuated subgenome-length minus-strand RNAs would serve directly as templates for transcription of mRNA. Adapted from reference 37.

Citation: Perlman S, Gallagher T, Snijder E. 2008. Color Plates, In Nidoviruses. ASM Press, Washington, DC.
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Image of Color Plate 3 (chapter 7).

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Color Plate 3 (chapter 7).

Colocalization of nidovirus replicase proteins and viral RNA visualized by immunofluorescence assays. EAV, EAV-infected BHK-21 cells at 10 h postinfection. (A) Detection of EAV nsp3, one of the viral replicase TM proteins, using specific antiserum. (B) In situ hybridization using a fluorescently labeled RNA probe complementary to a part of the EAV replicase gene, and thus recognizing genome-length plus-strand RNA. (C) Overlay showing colocalization of nsp3 and plus-strand RNA. (Courtesy of Yvonne van der Meer, Jessika Zevenhoven-Dobbe, and Eric Snijder, Leiden University Medical Center, Leiden, The Netherlands). MHV, MHV-A59-infected 17cl-1 cells at 8.5 h postinfection. (D) Detection of MHV nsp5 (3CL) using specific antiserum. (E) Detection of newly synthesized viral RNA labeled with BrUTP in the presence of actino-mycin D, using antiserum directed against BrdU. (F) Overlay showing colocalization of nsp5 and newly synthesized viral RNA (reproduced with permission from Shi et al., 1999). SARS-CoV, SARS-CoV-infected Vero-E6 cells. (G) Detection of nsp3 using specific antiserum. (H) Detection of newly synthesized viral RNA labeled with BrUTP in the presence of actinomycin D, using antiserum directed against BrdU. (I) Overlay showing colocalization of nsp3 and newly synthesized viral RNA (reproduced with permission from reference 25.)

Citation: Perlman S, Gallagher T, Snijder E. 2008. Color Plates, In Nidoviruses. ASM Press, Washington, DC.
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Image of Color Plate 4 (chapter 10).

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Color Plate 4 (chapter 10).

Cocrystal of the SARS-CoV RBD bound to human ACE2. (A) The RBD of SARS CoV, residues 319 to 511, is shown in red, bound to the ectodomain of human ACE2, shown in white. ACE2 regions that contact the SARS-CoV RBD are indicated in orange ribbon. Residues within these same regions also contribute to HCoV-NL63 entry, indicating substantial overlap between HCoV-NL63 and SARS-CoV binding regions on ACE2. SARS-CoV RBD residues 479 and 487, whose alteration from lysine to asparagine and serine to threonine, respectively, permits efficient use of human ACE2, are shown in green. ACE2 lysine 31, which precludes association with S proteins bearing lysine 479, found in most palm civet viruses, is shown in magenta. ACE2 threonine 487, critical for efficient use of human and palm civet ACE2, and found only in SARS-CoV isolated from humans during the 2002-2003 epidemic, is shown in green. Lysine 353 is shown in cyan. (B) Closeup view of the ACE2-RBD contact region, in which RBD residues other than 479 and 487 are hidden. Note the close contact between the methyl group of threonine 487 of the RBD and the stalk of ACE2 lysine 353, critical to SARS-CoV entry.

Citation: Perlman S, Gallagher T, Snijder E. 2008. Color Plates, In Nidoviruses. ASM Press, Washington, DC.
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Image of Color Plate 5 (chapter 19).

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Color Plate 5 (chapter 19).

Histopathology of SARS-CoV lung infection. (A) Hematoxylin and eosin stain showing the early phase of SARS pneumonia; pink hyaline membranes within the alveoli and increased inflammatory cells in the interstitium can be seen. (B) Hematoxylin and eosin stain showing the organizing phase of SARS. There is obliteration of the alveoli by fibrous tissue and reactive pneumocytes. A giant cell is identified in the center of the field. (C) AEC (3-amino-9-ethylcarbazole) with hematoxylin counterstain immunochemistry for SARS-CoV nucleoprotein in early-stage SARS pneumonia; positive staining for nucleoprotein in flattened pneumocytes can be seen. (D) AEC with hematoxylin counterstain immunochemistry for SARS-CoV nucleoprotein in early-stage SARS pneumonia with evidence that the carbon-containing macrophages are also positive for SARS nucleoprotein. (E) AEC with hematoxylin counterstain showing early SARS pneumonia; shown are results of in situ hybridization with pooled SARS-CoV genes, with red positive staining of the bronchial epithelium, flattened pneumocytes, and macrophages. Magnification for all panels, X200.

Citation: Perlman S, Gallagher T, Snijder E. 2008. Color Plates, In Nidoviruses. ASM Press, Washington, DC.
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Image of Color Plate 6 (chapter 22).

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Color Plate 6 (chapter 22).

Critical immune parameters controlling MHV infection within the CNS during the innate (A), acute (B), and persistent (C) stages of infection. Crucial effector molecules are boxed for each phase. (A) Infection by the MHV-JHM variant V2.2-1 is initiated in ependymal cells and spreads to glial cells, but only rarely to neurons. Microglia (Mic), macrophages (Mac), and astrocytes (Ast) are infected prior to oligodendrocytes (Olg), the cell type maintaining myelin and thus axonal function. Early viral replication induces expression of MMP-3 and MMP-12, as well as numerous chemokines (green) and cytokines (purple). The earliest chemokines detected are CCL3, CXCL1, and CXCL10. Neutrophils (N) and monocytes/macrophages (Mac) are recruited from the bone marrow (BM) as an integral part of the acute-phase response. By releasing MMP-9, N enhance breakdown of the extracellular matrix and facilitate subsequent entry of lymphocytes. Induction of type I IFN (boxed) is critical to stem initial viral spread, prior to expansion and recruitment of antiviral T cells. The extent to which DC subsets contribute to IFN-α/β secretion in lymphoid tissue is being investigated rigorously. Similarly, the migration pattern of DC detected in the CNS and CLN, as well as their acquisition of viral antigen, remains to be elucidated. (B) Viral antigen presentation in lymphoid tissue results in activation, expansion, and extravasation of virus-specific CD8 and CD4 T cells. Proinflammatory cytokines and chemokines act as guiding signals for recruitment to the site of infection. While CD8 T cells localize to parenchymal CNS sites, CD4 T cells initially remain perivascular, correlated with TIMP-1 production. CD8 T cells exert antiviral function via IFN-γ and perforin-mediated cytolytic pathways. IFN-γ is critical in control of viral replication and host survival, presumably by enhancing MHC molecule antigen presentation. The apparent resistance of oligodendrocytes to both perforinmediated viral clearance and infection-induced apoptosis, contrasting with disintegration of myelin sheaths, remains an enigma. Nevertheless, T-cell effector function is tightly associated with macrophage/microglial activation and uptake of myelin debris. As T cells are recruited, viral replication diminishes and levels of MMPs, chemokines, and innate cytokines decline. CCL5 and CXCL10 expression remains prominent. (C) Despite control of infectious virus, virus persists in astrocytes and oligodendrocytes. There is little evidence of an antiviral role for T cells retained or still recruited during persistence, as cytolytic activity is lost and IFN-γ secretion is significantly reduced. Local Ab prevents viral recrudescence, which is achieved by accumulation and retention of virus-specific ASC (vASC). Accumulation of vASC in BM is modest, suggesting preferential recruitment to the CNS. Continued CXCL10 and up-regulation of the B-cell survival factor BAFF might underlie ongoing B-cell/ASC recruitment, differentiation, and survival. The vital humoral component keeping persistent virus in check is neutralizing Ab (nAb).

Citation: Perlman S, Gallagher T, Snijder E. 2008. Color Plates, In Nidoviruses. ASM Press, Washington, DC.
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Image of Color Plate 7 (chapter 23).

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Color Plate 7 (chapter 23).

Schematic representation of the typical extracellular morphology of torovirus (as visualized by EM) and its structural proteins and genome (single-stranded RNA of positive polarity, polyadenylated tail, and six open reading frames).

Citation: Perlman S, Gallagher T, Snijder E. 2008. Color Plates, In Nidoviruses. ASM Press, Washington, DC.
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Image of Color Plate 8 (chapter 24).

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Color Plate 8 (chapter 24).

Gross signs of YHD in the giant tiger shrimp The three diseased shrimp to the left display bleached yellowish discoloration of the cephalothorax caused by paleness of the underlying hepatopancreas and brownish discoloration of the gills. Photograph kindly supplied by T. W. Flegel, CENTEX Shrimp, Mahidol University, Bangkok, Thailand.

Citation: Perlman S, Gallagher T, Snijder E. 2008. Color Plates, In Nidoviruses. ASM Press, Washington, DC.
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