interferon

Interferons (IFNs) were first discovered in 1957 by Isaacs and Lindenman as an activity which was inducible by heat killed influenza virus in chick chorioallantoic membranes and could potently inhibit infection of fresh chick chorioallantoic membranes with live virus. It is composed of a family of distinct, acid stabile proteins which are highly similar in amino acid sequence and structure.

Persons with disorders of the interferon system are more susceptible to viral and bacterial diseases. Those with interferon production deficiencies are more susceptible to diseases caused by viruses such as HBV. Chronic hepatitis B virus infection acquired in later life is also associated with a defect in interferon production. Patients with defects in IFNα, IFNβ and IFNλ, production or action are exquisitely susceptible to viral diseases such as herpes simplex encephalitis.

Presently, interferons are classified into three major groups distinguished by their structure, receptor usage and downstream effects. Type I (α, β and ω) IFNs are produced by leukocytes (α) and most cells (β) as a direct response to viral infection. There are 14-20 IFNα genes in mammals, but only one IFNβ gene. Type I IFNs are comprised of at least 12 functional IFN-α’s, one IFN-β, and one IFN-ω species in human. Despite the large number of type I IFNs, they share a common receptor known as the type I IFN receptor (IFNAR), and activate the same signal transduction pathways to induce transcription of IFN-stimulated genes. They are also distinguishable by their sites of production. Type I IFNs are induced and secreted within hours after viral infection and thus they are a principal component of the innate immune response to viral infection.
Source: http://www.creativebiomart.net/r ... s-proteins_1230.htm