Viral evasion of interferon stimulated genes

Abstract

Viruses and their hosts since the dawn of time have been battling for supremacy. In recent years, the ‘Interferon Gateway’ encompassing interferon-alpha and -beta (IFN-a/b) expression, signalling and antiviral responses, has been uncovered. IFN-a/b are cytokines that coordinate the innate and adaptive immune responses to eliminate virus infections from the host. Interferon Stimulated Gene (ISG) products, such as protein kinase R, can prevent the translation of viral and cellular mRNAs to limit viral replication and can also initiate apoptosis if the cell is overwhelmed. In order to replicate, viruses have evolved viral evasion proteins that are able to target all aspects of the host response through a variety of sophisticated mechanisms. Viral evasion proteins can encode cellular domains to interact directly with ISGs and neutralize their function, hijack cellular pathways or degrade antiviral components. The high mutation rates associated with viral replication ensure that viruses will continue to adapt to our defences, but equally the viral evasion proteins are novel drug targets for eliminating or managing virus infections.