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Mechanism Of SARS Lung Damage Identified

Date:
February 5, 2008
Source:
American Society for Biochemistry and Molecular Biology
Summary:
Researchers have uncovered the mechanism that contributes to the buildup of fibrous lung tissue in patients with severe acute respiratory syndrome (SARS), finding that a SARS viral protein important for replication can enhance pulmonary fibrosis by inhibiting the activity of the enzyme that breaks down connective tissue. The results offer up a new pathway to treat the pulmonary damage of SARS.
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Immunohistochemical staining of normal (left) and SARS-infected (right) lung tissue reveals excess fibrous tissue buildup due to activation of plasminogen inhibitor PAI-1 (blue).
Credit: Journal of Biological Chemistry

Researchers have uncovered the mechanism that contributes to the buildup of fibrous lung tissue in patients with severe acute respiratory syndrome (SARS), finding that a SARS viral protein important for replication can enhance pulmonary fibrosis by inhibiting the activity of the enzyme that breaks down connective tissue.

The results offer up a new pathway to treat the pulmonary damage of SARS.

Infection with the SARS virus can lead to severe inflammation in the lungs, which can lead to respiratory distress, fibrosis, and eventually lung failure. Ye-Guang Chen and colleagues tested the effect of a SARS viral protein, the nucleocapsid protein (the protein that binds the virus's genetic material), on human lung cells and found that this protein can bind to a cellular protein called Smad3.

By associating with Smad3, the nucleocapsid protein accomplishes two things. First, it prevents Smad3 from binding to its partner Smad4 and initiating cell suicide, allowing the virus to replicate longer. At the same time, Smad3-Nucleocapsid binding stimulates a separate pathway that promotes the production of collagen and an inhibitor (PAI-1) of the plasminogen protein, which breaks down non-cell materials and other build-up in the body, leading to lung fibrosis.

So, in a trade-off, the SARS virus increases its short-term gain at the expense of long-term damage to its host.

This research was recently published in the Journal of Biological Chemistry. Corresponding Author: Ye-Guang Chen, Department of Biological Sciences and Biotechnology, Tsinghua University.


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The above story is based on materials provided by American Society for Biochemistry and Molecular Biology. Note: Materials may be edited for content and length.


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American Society for Biochemistry and Molecular Biology. "Mechanism Of SARS Lung Damage Identified." ScienceDaily. ScienceDaily, 5 February 2008. <www.sciencedaily.com/releases/2008/02/080201131541.htm>.
American Society for Biochemistry and Molecular Biology. (2008, February 5). Mechanism Of SARS Lung Damage Identified. ScienceDaily. Retrieved May 24, 2015 from www.sciencedaily.com/releases/2008/02/080201131541.htm
American Society for Biochemistry and Molecular Biology. "Mechanism Of SARS Lung Damage Identified." ScienceDaily. www.sciencedaily.com/releases/2008/02/080201131541.htm (accessed May 24, 2015).

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