SARS MODEL
Severe acute respiratory syndrome (SARS) first emerged in Hong Kong in November 2002 and quickly spread to Canada, Singapore, and Vietnam, resulting in over 8,000 cases and 774 deaths. The syndrome was characterized by a rapidly progressive pneumonia, and scientists from all over the world began working at phenomenal speeds to understand the cause of illness and prevent its spread. With this intense collaborative effort, the identification of a novel coronavirus (SARS-CoV), as well as the sequencing of its genome, was accomplished in only five weeks. The outbreak was brought under control with public health measures that included quarantine and travel advisories.
Despite this early success, developing an adequate animal model for SARS has remained a challenge, and none of the available models fully replicate the severe disease seen in humans. Studies from different laboratories have shown that cynomolgus and rhesus macaques can be experimentally infected with SARS-CoV, although the severity of lung pathology and clinical signs has varied. Nevertheless, the macaque model most adequately mirrors many aspects of SARS-CoV infection in humans, including infection of bronchial epithelial cells and type-1 and type-2 pneumoctyes and diffuse alveolar damage, characterized by the loss of epithelium from alveolar and bronchial walls. Virus replication is prevalent within the lung and significant changes in host gene expression due to SARS-CoV infection can be identified. The ability to examine gene expression changes in the lungs of these animals holds great promise for providing insights into the mechanisms of innate immunological responses and SARS-CoV mediated lung injury. Our studies using the macaque model for SARS are conducted in collaboration with Dr. Albert D.M.E. Osterhaus (Erasmus Medical Center, Rotterdam, Netherlands) and Dr. Ralph Baric (University of North Carolina).