Inhibitor of NF kappa B alpha is a host sensor of coxsackievirus infection.

Abstract

Apoptosis is a host response to viral infection: programmed cell death can limit viral replication. Therefore, the knowledge of pathways by which cells detect viral infection and activate apoptosis may be of considerable interest when developing strategies against viral pathogens. We have shown that cells activate apoptosis in response to Coxsackievirus B3 (CVB3) infection. In an effort to discover how cells detect viral infections, we found that the viral protease 3C(pro) cleaves IkappaBalpha. Truncated IkappaBalpha forms a stable complex with NFkappaB, translocates to the nucleus and inhibits NFkappaB transactivation, increasing apoptosis and decreasing viral replication. In contrast, cells in which IkappaBalpha expression is reduced are more susceptible to viral infection, showing less apoptosis and more viral replication. IkBalpha 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.

• Authors: Marta Saura, Tania R Lizarbe, Concepción Rama-Pacheco, Charles J Lowenstein, Carlos Zaragoza
• Journal: Cell cycle (Georgetown, Tex.) (Cell Cycle) Vol. 6 Issue 5 Pg. 503-6 (Mar 01 2007) ISSN: 1551-4005 [Electronic] United States
• PMID: 17351338 (Publication Type: Comparative Study, Journal Article)

Chemical References

• I-kappa B Proteins
• NFKBIA protein, human
• NF-KappaB Inhibitor alpha

Topics

• Apoptosis (physiology)
• Coxsackievirus Infections (metabolism, pathology, virology)
• Enterovirus B, Human (pathogenicity)
• HeLa Cells
• Humans
• I-kappa B Proteins (physiology)
• NF-KappaB Inhibitor alpha
• Virus Activation (physiology)