Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 103, Issue 50, Pages 19051-19056Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0606019103
Keywords
Coxsackievirus; nitric oxide; Picornavirus
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Apoptosis is an innate immune response to viral infection that limits viral replication. However, the mechanisms by which cells detect viral infection and activate apoptosis are not completely understood. We now show that during Coxsackievirus infection, the viral protease 3C(pro) cleaves inhibitor of kappa B alpha (I kappa B alpha). A proteolytic fragment of I kappa B alpha then forms a stable complex with NF-kappa B, translocates to the nucleus, and inhibits NF-kappa B transactivation, increasing apoptosis and decreasing viral replication. In contrast, cells with reduced I kappa B alpha expression are more susceptible to viral infection, with less apoptosis and more viral replication. I kappa B alpha thus acts as a sensor of viral infection. Cleavage of host proteins by pathogen proteases is a novel mechanism by which the host recognizes and responds to viral infection.
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