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BMC Genomics  2005 

Molecular signature of clinical severity in recovering patients with severe acute respiratory syndrome coronavirus (SARS-CoV)

DOI: 10.1186/1471-2164-6-132

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Based on changes in gene expression of peripheral blood, we identified 52 signature genes that accurately discriminated acute SARS patients from non-SARS controls. While a general suppression of gene expression predominated in SARS-infected blood, several genes including those involved in innate immunity, such as defensins and eosinophil-derived neurotoxin, were upregulated. Instead of employing clustering methods, we ranked the severity of recovering SARS patients by generalized associate plots (GAP) according to the expression profiles of 52 signature genes. Through this method, we discovered a smooth transition pattern of severity from normal controls to acute SARS patients. The rank of SARS severity was significantly correlated with the recovery period (in days) and with the clinical pulmonary infection score.The use of the GAP approach has proved useful in analyzing the complexity and continuity of biological systems. The severity rank derived from the global expression profile of significantly regulated genes in patients may be useful for further elucidating the pathophysiology of their disease.SARS-CoV is a single-stranded, plus-sense RNA virus with a genome of ~30 kb. Its sequence does not closely resemble any of the previously characterized coronaviruses [1-4]. Before SARS-CoV was recognized as the cause of the deadly SARS [1-3,5-7], other human coronaviruses had only been known to account for 15–30% of colds [8]. SARS-CoV appears to be new to humans, as supported by the finding that human sera collected before the SARS outbreak did not contain antibodies against this virus [3,9]. After an incubation period from 2 to 10 days, SARS patients might develop fever (>38°C), headache, dry cough, and pneumonia [3,5,9-14]. Most patients gradually recovered while some progressed to respiratory distress syndrome with ~10% mortality rate. The genome-wide changes in human gene expression when challenged by this novel pathogen are essentially unknown.Profiles of gene exp


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