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J. Biol. Chem., Vol. 280, Issue 25, 24153-24158, June 24, 2005

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Proteolytic Cleavage of the p65-RelA Subunit of NF-B during Poliovirus Infection^*

Nickolay Neznanov, Konstantin M. Chumakov¶, Lubov Neznanova, Alexandru Almasan||, Amiya K. Banerjee, and Andrei V. Gudkov**

From the Departments of Molecular Genetics and ^||Cancer Biology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195 and the ^¶Center for Biologics Evaluation and Research, United States Food and Drug Administration, Rockville, Maryland 20852

Activation of NF-B during viral infection is one of the critical elements in innate immune response. Several virus-specific factors, such as double-stranded RNA, can trigger host defense mechanisms by inducing NF-B-mediated expression of cytokines and interferons. Early stages of poliovirus infection are also associated with degradation of IB and translocation of NF-B into the nucleus. However, at later stages of poliovirus replication the p65-RelA component of the NF-B complex undergoes a specific cleavage that coincides with the onset of intensive poliovirus protein synthesis and the appearance of the activity of poliovirus protease 3C. Indeed, the p65-RelA amino acid sequence contains the recognition site for 3C, and recombinant protein 3C was shown to be capable of proteolytic cleavage of p65-RelA, generating truncated product similar to that observed during poliovirus infection. Cleavage of p65-RelA occurs during replication of ECHO-1 and rhinovirus 14, suggesting that inactivation of NF-B function by proteolytic cleavage of p65-RelA is the common mechanism by which picornaviruses suppress the innate immune response.

Received for publication, March 1, 2005 , and in revised form, April 20, 2005.

^* This work was supported by National Institutes of Health Grants CA60730 and CA88071 (to A. V. G.), by a grant from the American Cancer Society, Illinois Division, and by funds provided by the Lerner Research Institute (to N. N.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence may be addressed. Tel.: 216-444-1058; Fax: 216-444-2998; E-mail: neznann{at}ccf.org.

^** To whom correspondence may be addressed. Tel.: 216-445-1205; Fax: 216-444-2998; E-mail: Gudkov{at}ccf.org.

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