BackgroundSevere acute respiratory syndrome (SARS), a recent epidemic human disease, is caused by a novel coronavirus (SARS-CoV). First reported in Asia, SARS quickly spread worldwide through international travelling. As of July 2003, the World Health Organization reported a total of 8,437 people afflicted with SARS with a 9.6% mortality rate. Although immunopathological damages may account for the severity of respiratory distress, little is known about how the genome-wide gene expression of the host changes under the attack of SARS-CoV.ResultsBased 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.ConclusionThe 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.
Background: Persistent impaired pulmonary function and functional capacity are common among survivors of severe acute respiratory syndrome (SARS). Whether the impairment was caused by SARS or pre-existing physical condition remains unclear. Objective: This study investigated the influence of SARS on exercise capacity and pulmonary function of previously healthy medical staff.Methods: Pulmonary function tests, including spirometry and carbon monoxide diffusing capacity (DLCO), as well as symptom-limited cardiopulmonary exercise testing (CPET) with an incremental protocol using an electronically braked cycle ergometer, were performed by 13 previously healthy hospital workers 14 months after SARS recovery. Other 14 age- and sex-matched healthy medical workers completed CPET simultaneously, and exercise capacities of these two groups were compared. Results: Most values of spirometry performed were within normal range. Only one showed mildly restrictive abnormality with decreased forced expiratory volume in 1 s (72.2% predicted) and forced vital capacity (68.1% predicted). Eight subjects had decreased DLCO levels (mean 79.37 ± 7.73%), and low exercise capacity was noted in 9 subjects. Discordance in impairment of the measured DLCO and exercise capacity was revealed by comparison. Besides, there was no significant difference in results of CPET between subjects recovered from SARS and those never infected. Conclusions: Minor pulmonary function defects as well as decreased exercise capacity were detected in previously healthy medical staff after recovering from SARS. No significant correlation between exercise capacity and pulmonary function was found.
Old age, high white blood cell counts, high peak grade fever, and close or prolonged contact with a SARS patient increase the risk of intubation in previous healthy SARS patients.
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