Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2007 Apr;1102(1):86-95.
doi: 10.1196/annals.1408.006.

Signal transduction in SARS-CoV-infected cells

Affiliations
Review

Signal transduction in SARS-CoV-infected cells

T Mizutani. Ann N Y Acad Sci. 2007 Apr.

Abstract

Severe acute respiratory syndrome (SARS) is a newly found infectious disease that is caused by a novel human coronavirus, SARS coronavirus (SARS-CoV). Because the mortality rate of SARS patients is very high, understanding the pathological mechanisms of SARS not only in vivo but in vitro is important for the prevention of SARS. Activation of signaling pathways caused by SARS-CoV infection leads to the phosphorylation and activation of downstream molecules. Two conflicting cellular programs, apoptosis to eliminate virus-infected cells and survival to delay apoptosis by producing antiviral cytokines, occur in SARS patients. Recent studies regarding SARS and SARS-CoV have clarified that activation of mitogen-activated protein kinases (MAPKs) plays important roles in upregulation of cytokine expression and apoptosis both in vitro and in vivo. Both Akt and p38 MAPK are keys for determination of cell survival or death in SARS-CoV-infected cells in vitro. Agents being developed to target these signaling cascades may be important for the design of anti-SARS-CoV drugs. This review highlights recent progress regarding SARS-CoV biology, especially signal transduction in SARS-CoV-infected cells.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic representation of signal transduction on SARS‐CoV infection.

Similar articles

Cited by

References

    1. Banerjee, S. , Narayanan K., Mizutani T. & Makino S.. 2002. Murine coronavirus replication‐induced p38 mitogen‐activated protein kinase activation promotes interleukin‐6 production and virus replication in cultured cells. J. Virol. 76: 5937–5948. - PMC - PubMed
    1. Cardone, M.H. , Roy N., Stennicke H.R., et al 1998. Regulation of cell death protease caspase‐9 by phosphorylation. Science 282: 1318–1321. - PubMed
    1. Chang, L. & Karin M.. 2001. Mammalian MAP kinase signalling cascades. Nature 410: 37–40. - PubMed
    1. Chang, Y.J. , Liu C.Y., Chiang B.L., et al 2004. Induction of IL‐8 release in lung cells via activator protein‐1 by recombinant baculovirus displaying severe acute respiratory syndrome‐coronavirus spike proteins: identification of two functional regions. J. Immunol. 173: 7602–7614. - PubMed
    1. Cheung, C.Y. , Poon L.L., Ng L.H., et al 2005. Cytokine responses in severe acute respiratory syndrome coronavirus‐infected macrophages in vitro: possible relevance to pathogenesis. J. Virol. 79: 7819–7826. - PMC - PubMed

Publication types

MeSH terms

-