Signaling pathways of SARS-CoV in vitro and in vivo

Abstract

Severe acute respiratory syndrome (SARS) is a respiratory illness with variable symptoms that was recognized as the first near-pandemic infectious disease of the twenty-first century. A novel human coronavirus, named SARS coronavirus (SARS-CoV), derived from SARS patients was reported as the etiologic agent of SARS. Studying the signaling pathways of SARS-infected cells is key to understanding the molecular mechanism of SARS viral infection. Cell death is observed in cultured Vero E6 cells after SARS-CoV infection. From SARS-CoV infection to cell death, p38 mitogen-activated protein kinase (MAPK) is a key participant in the determination of cell death and survival. Two signaling pathways comprising signal transducer and activator of transcription 3 (STAT3) and p90 ribosomal S6 kinase (p90RSK) are downstream of p38 MAPK. AKT and JNK (Jun NH2-terminal kinase) signaling pathways are important to establish persistent infection of SARS-CoV in Vero E6 cells. Expression studies of SARS-CoV proteins indicate that the viral proteins are able to activate signaling pathways of host cells. The study of signaling pathways in SARS-CoV patients is difficult to perform compared with in vitro studies due to the effects of the human immune system. This review highlights recent progress in characterizing signal transduction pathways in SARS-CoV-infected cells in vitro and in vivo. © 2010 Springer-Verlag Berlin Heidelberg.