Viral Protein Stops Inflammatory Response

A viral protein has been found that inactivates the immune system's anti-inflammatory response mechanism, which shields the virus from immune attack but may be exploited as a drug to treat inflammatory diseases of the skin.

Investigators at the University of Illinois (Urbana-Champaign, USA) worked with the molluscum contagiosum virus (MCV), which causes a mild skin disease similar to chickenpox. In particular they focused their attention on the product of the viral MC160 gene, which has a homologue in humans and in herpes viruses, that regulates the cellular transcription factor NF-kappaB. NF-kappaB is activated when cytokine tumor necrosis factor alpha (TNF-alpha) binds to its cognate, TNF receptor I.

Studies on the effect of the MC160 protein on T cells growing in culture showed that it significantly reduced TNF-alpha-mediated NF-kappaB activation. MC160 protein expression reduced IKK kinase activity and IKK subunit phosphorylation. This is a step common to multiple signal transduction pathways. These findings were published in the January 2006 issue of the Journal of Virology.

"Our findings regarding MC160 provide yet another example of how viruses inhibit NF-kappaB activation,” explained senior author Dr. Joanna L. Shisler, professor of microbiology at the University of Illinois. "So we are starting to get a broader feeling that there is a common mechanism, that of inhibiting NF-kappaB activity, that all viruses are trying to utilize to survive in the host. What is interesting is that MC160 appears to be doing it in a completely novel way, than any identified before, by focusing on this IKK complex. This virus makes other proteins that dampen the immune response, but MC160 seems to be an important one.”



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