Pathogenesis of severe acute respiratory syndrome

• 作 者: ZHANG Ding-mei LU Jia-hai ZHON
• 机 构: School of Public Health,Guangzhou Institute of Respiratory Diseases
• 出 处: 中华医学杂志（英文版）
• 发表日期: 2004年期
• 关键词: pathogenesis severe acute respiratory syndrome

Severe acute respiratory syndrome (SARS) first emerged in Guangdong province,China in November2002.During the following 3 months,it spread rapidly across the world,resulting in approximately 800 deaths.In 2004,subsequent sporadic cases emerged in Singapore and China.A novel coronavims,SARS-CoV,was identified as the etiological agent of SARS.1,2 This virus belongs to a family of large,positive,single-stranded RNA viruses.Nevertheless,genomic characterization shows that the SARS-CoV is only moderately related to other known coronaviruses.3 In contrast with previously described coronaviruses,SARS-CoV infection typically causes severe symptoms related to the lower respiratory tract.The SARS-CoV genome includes 14 putative open reading frames encoding 28 potential proteins,and the functions of many of these proteins are not known.4 A number of complete and partial autopsies of SARS patients have been reported since the first outbreak in 2003.The predominant pathological finding in these cases was diffuse alveolar damage (DAD).This severe pulmonary injury of SARS patients is caused both by direct viral effects and immunopathogenetic factors.5 Many important aspects of the pathogenesis of SARS have not yet been fully clarified.In this article,we summarize the most important mechanisms involved in the complex pathogenesis of SARS,including clinical characters,host and receptors,immune system response and genetic factors.