Antiviral state

The antiviral state limits the host cell's ability to support viral replication by reducing the cell's ability to make protein. It requires dsRNA as the viral genome or replication intermediate.

IFN-α/-β released by viral-infected cells bind to nearby cells expressing a common IFN-α/-β receptor. Receptor engagement triggers a signalling cascade, inducing the transcription of IFN-stimulated genes.

Two important antiviral proteins are produced: 2',5'-oligoA synthetase (2',5'-OAS) and '''dsRNA dependent protein kinase (PKR). '''The activities of these molecules inhibit the synthesis of both host and viral proteins.

2', 5'-OAS
2',5'-OAS enzyme activates RNase-L, which degrades mRNAs, both cellular and viral.

PKR
Activated PKR inactivates eIF-2, an essential factor in translation.