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2 : Severe Acute Respiratory Syndrome (SARS)

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Severe Acute Respiratory Syndrome (SARS), Page 1 of 2

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Abstract:

Severe acute respiratory syndrome (SARS) coronavirus (CoV) infection, in addition to infections originating in the laboratory, was detected in four patients with no possible laboratory exposure during December 2003 and January 2004. These four epidemiologically unrelated patients likely acquired the infection through exposure to infected animals in live-game-animal markets in Guangdong. A number of possible agents were detected in the course of investigating patients with suspected SARS, including human metapneumovirus and chlamydia. In the absence of an epidemiological history of exposure, clinical findings are not pathognomic of SARS. Therefore, a positive virological laboratory finding of SARS CoV infection is required for confirmation of the diagnosis. Evidence of SARS CoV replication in the lungs and intestine is provided by detection of virus particles through electron microscopy, by virus isolation, and by the detection of viral antigens and nucleic acid through immunohistology and in situ hybridization. Experimental infections in relevant animal models are important for understanding pathogenesis and evaluating therapeutic and vaccine strategies. The clinical management of patients with SARS includes respiratory support with intensive care when appropriate, prevention of nosocomial transmission, and the possible use of antivirals and immunomodulators. Aspects of its pathogenesis and transmission allowed the human disease outbreak to be quickly interrupted. The global response to SARS demonstrated that a rapid mobilization and coordination of relevant expertise is possible, when faced with a global emerging disease threat. It also highlighted the need for improved international regulations governing the reporting of and response to unusual infectious-disease syndromes.

Citation: M. Peiris J, Guan Y, M. Poon L, C. Cheng V, Nicholls J, Yuen K. 2007. Severe Acute Respiratory Syndrome (SARS), p 23-50. In Scheld W, Hooper D, Hughes J (ed), Emerging Infections 7. ASM Press, Washington, DC. doi: 10.1128/9781555815585.ch2
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Figures

Image of Figure 1.
Figure 1.

(Top) SARS CoV-infected FRhK-4 cells showing newly formed virus particles. (Bottom) Schematic view of a SARS CoV particle. The four structural proteins, spike, envelope, membrane, and nucleocapsid, and the viral genomic RNA are indicated. Within the virion, the viral RNA is encapsulated with nucleoprotein (shown in part). The drawing is not to scale.

Citation: M. Peiris J, Guan Y, M. Poon L, C. Cheng V, Nicholls J, Yuen K. 2007. Severe Acute Respiratory Syndrome (SARS), p 23-50. In Scheld W, Hooper D, Hughes J (ed), Emerging Infections 7. ASM Press, Washington, DC. doi: 10.1128/9781555815585.ch2
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Image of Figure 2.
Figure 2.

(A) Phylogenetic analysis of RNA sequences coding for RNA-dependent RNA polymerase (partial sequence). Phylogenetic trees were constructed by the neighbor-joining method, and bootstrap values were determined by 1,000 replicates. Human SARS CoV (SARS-CoV) (GenBank accession number NC004718), SARS CoVs isolated from palm civets in 2003 (AY304487) and 2004 (AY686863) and SARS CoV-related virus from bats (Bat-SARS-CoV; DQ022305) were aligned with reference sequences as indicated. The reference sequences used in the study were transmissible gastroenteritis virus (TGEV) (NC002306), human coronavirus (HCoV) HCoV-229E (AF304460), HCoV-NL63 (AY567487), HCoV-OC43 (NC005147), HCoV-HKU1 (NC006577), porcine epidemic diarrhea virus (PEDV) (AF353511), infectious bronchitis virus (IBV) (NC005147), mouse hepatitis virus (MHV) (NC001846), and group 1 Bat-CoV (AY864196). (B) Genome organization of SARS CoV. ORFs 1 to 9 are indicated. Polyproteins encoded by ORFs 1a and 1b are cleaved by papain-like cysteine proteinase (nsp 3) and 3C-like cysteine proteinase (nsp 5) to generate 16 nonstructural polyproteins (nsp 1 to 16). The cleavage sites for papain-like cysteine proteinase and 3C-like cysteine proteinase are indicated by gray and black arrows, respectively. ORFs 2, 4, 5, and 9a encode the viral structural proteins, S, E, M, and N, respectively. Subgenomic mRNAs 3, 7, 8, and 9 are believed to express two viral proteins.

Citation: M. Peiris J, Guan Y, M. Poon L, C. Cheng V, Nicholls J, Yuen K. 2007. Severe Acute Respiratory Syndrome (SARS), p 23-50. In Scheld W, Hooper D, Hughes J (ed), Emerging Infections 7. ASM Press, Washington, DC. doi: 10.1128/9781555815585.ch2
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Image of Figure 3.
Figure 3.

Chest radiographs (A and B) and high-resolution CT scans (C to E) from two SARS patients. (Courtesy of C. M. Chu. Reproduced with permission from reference .) (A) Chest radiograph of a man aged 34 years at day 7 of illness, with consolidation in the left upper and middle lobes. (B) By day 20, resolution of consolidation in the left upper and middle lobes and new widespread air space opacities were noted. Those in the left lung base were confluent. (C) High-resolution CT scan of a man aged 32 years who presented with fever, chills, rigor, and myalgia with a clear chest radiograph at admission, demonstrating peripheral subpleural consolidation in the medial basal segment of the left lower lobe. (D) At day 18, there was resolution of the original left lower lobe consolidation. (E) Disease was complicated by spontaneous pneumomediastinum.

Citation: M. Peiris J, Guan Y, M. Poon L, C. Cheng V, Nicholls J, Yuen K. 2007. Severe Acute Respiratory Syndrome (SARS), p 23-50. In Scheld W, Hooper D, Hughes J (ed), Emerging Infections 7. ASM Press, Washington, DC. doi: 10.1128/9781555815585.ch2
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