Human IFN-alpha proteins are found as multiple subtypes produced by a viral infection, immune stimulators, and chemical inducers. These type I interferon alpha proteins differentially exhibit antiviral, antiproliferative and immunomodulatory activities. When interferon alpha interacts with its cognate receptor, a signal is rapidly transmitted within the cell, often producing an antiviral state. The primary signal transduction cascade promoted by type I interferons is the JAK1-STAT pathway. Activation of this cascade leads to increased expression of a large number of genes, including (2'-5') oligoadenylate synthetases, Mx proteins, and protein kinase R (PKR) that protect the cell from viral infection. Interferon Alpha 2a and Alpha 2b are the most widely used therapeutic interferon alpha proteins, and have been modified with polyethylene glycol sidechains to yield therapeutic interferons with extended half-lives. First approved for the treatment of Hairy Cell Leukemia, interferon alpha has been utilized extensively as a therapeutic intervention to treat patients with Hepatitis B, Hepatitis C, Melanoma, and T-cell Lymphoma. Though the detailed biological mechanisms responsible for the actual and potential therapeutic activities and varied biological sequelae of each of the type I interferon alpha subtypes are not well defined in most cases, this family of interferon proteins comprises an important area of life science and therapeutic investigation.

 

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