The Animal Model And The Pathogenesis Of Lung Damage On SRAS-CoV Infection

Severe Acute Respiratory Syndrome (SARS), a novel human infectious disease with high fatality has spread globally since November 2002, starting in Guangdong Province, China. Since then great attention has been paid internationally to the infection, and 8,437 cases with 813 fatal cases appeared as of July 11, 2003. Including 5,327 cases with 348 dead were reported in the Mainland China. In March 2003, the World Health Organization (WHO) launched an alert of the disease named SARS. A collaborative researches and supervision networks involving 10 countries and 13 laboratories have been established. The severely affected patients exhibited an acute respiratory distress syndrome, and some developed multiple organ failures (MOF). Pathology revealed severe hepatization of the lung together with structural damage in multiple organs including heart, spleen, liver and kidney. The lungs from severely SARS patients show three types of lesions, diffuse edema with the formation of the lucid membrane (fatal in 1 to 2 weeks), wide spread necrosis with desquamated epithelium (fatal in 3 to 4 weeks) and early fibrosis (fatal in 5 to 6 weeks). The changes are progressive and staggered. The spleen and lymph nodes have apoptosis, necrosis and hemorrhage, followed by regeneration. SARS-CoV is tropic for the vascular epithelial cells, alveolar epithelial cells and lymphoid cells, probably related to the ACE2 receptors, which is the function receptor of SARS-CoV. The animal models have been required for exploring the pathogenesis and control of the viral disease. The establishment of SARS-CoV infected animal models has become a unanimously accepted target and it is a compulsory task and the prerequisite to the development of antiviral therapies and vaccines.Purpose: My aims are to establish animal models for SARS-CoV infection and to offer a platform for developing effective drugs and vaccines...