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A virus-infected cell releases viral particles that can infect nearby cells. However, the infected cell can protect neighboring cells against a potential infection of the virus by releasing interferons. In response to interferon, cells produce large amounts of an enzyme known as protein kinase R (PKR).
The type-I interferons (IFN) are cytokines which play essential roles in inflammation, immunoregulation, tumor cells recognition, and T-cell responses. In the human genome, a cluster of thirteen functional IFN genes is located at the 9p21.3 cytoband over approximately 400 kb including coding genes for IFNα (IFNA1, IFNA2, IFNA4, IFNA5, IFNA6, IFNA7, IFNA8, IFNA10, IFNA13, IFNA14, IFNA16 ...
Interferon beta-1a (also interferon beta 1-alpha) is a cytokine in the interferon family used to treat multiple sclerosis (MS). [5] It is produced by mammalian cells, while interferon beta-1b is produced in modified E. coli. [6] Some research indicates that interferon injections may result in an 18–38% reduction in the rate of MS relapses. [7]
Upon infection, STING from infected cells can sense the presence of nucleic acids from intracellular pathogens, and then induce interferon β and more than 10 forms of interferon α production. Type I interferon produced by infected cells can find and bind to Interferon-alpha/beta receptor of nearby cells to protect cells from local infection.
Interferon beta is a protein that in humans is encoded by the IFNB1 gene. [5] The natural and recombinant protein forms have antiviral, antibacterial, and anticancer properties. Interferon beta 1a (tradenames: Avonex and Rebif) and Interferon beta 1b (tradenames: Betaseron/Betaferon) are used as drugs.
When released, they signal to infected cells and other nearby cells that a pathogen is present. [9] This signal is passed from one cell to another by binding of the interferon to a cell surface receptor on a naïve cell. [10] The receptor and interferon are taken inside the cell while bound to initiate expression of ISGs. [10]
The interferon-α/β receptor (IFNAR) is a virtually ubiquitous membrane receptor which binds endogenous type I interferon (IFN) cytokines. Endogenous human type I IFNs include many subtypes, such as interferons-α, -β, -ε, -κ, -ω, and -ζ.
Interferon therapy, and specially interferon beta-1b, induces the production of neutralizing antibodies, usually in the second 6 months of treatment, in 5 to 30% of treated patients. [4] Moreover, a subset of RRMS patients with specially active MS, sometimes called "rapidly worsening MS" are normally non-responders to interferon beta-1b.