Proteolytic Cleavage of the p65-RelA Subunit of NF-κB during Poliovirus Infection

Activation of NF-κB 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-κB-mediated expression of cytokines and interferons. Early stages of poliovirus infect...

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Bibliographic Details
Published in:The Journal of biological chemistry 2005-06, Vol.280 (25), p.24153-24158
Main Authors: Neznanov, Nickolay, Chumakov, Konstantin M., Neznanova, Lubov, Almasan, Alexandru, Banerjee, Amiya K., Gudkov, Andrei V.
Format: Article
Language:English
Subjects:
Poliovirus
Rhinovirus
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Summary:Activation of NF-κB 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-κB-mediated expression of cytokines and interferons. Early stages of poliovirus infection are also associated with degradation of IκBα and translocation of NF-κB into the nucleus. However, at later stages of poliovirus replication the p65-RelA component of the NF-κB 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-κB function by proteolytic cleavage of p65-RelA is the common mechanism by which picornaviruses suppress the innate immune response.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M502303200