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Problematic sections in Wikipedia's INTERFERON entry
I have copied sections with problems and inserted my comments below.
Interferon therapy Diseases The immunomodulatory effects of interferons have been exploited to treat several diseases. Agents that activate the immune system, such as small imidazoquinoline molecules that activate TLR7, can induce IFN-α. Imidazoquinoline is the main ingredient of Aldara (Imiquimod) cream, a treatment approved in the United States by the Food and Drug Administration (FDA) for actinic keratosis, superficial basal cell carcinoma, papilloma and external genital warts. Synthetic IFNs are also made, and administered as antiviral, antiseptic and anticarcinogenic drugs, and to treat some autoimmune diseases. New research has shown that imiquimod's anti-proliferative effect is totally independent of immune system activation or function. Imiquimod exerts its effect by increasing levels of the opioid growth factor receptor (OGFr). Blocking OGFr function with siRNA technology resulted in loss of any antiproliferative effect of imiquimod.
Comment: The preceding two paragraphs are essentially advertising of a commercial product. Imiquimod is an insignificant therapeutic drug, which is rarely used. Reference 22 is twenty-six years old, certainly no longer “a current perspective”. I suggest deleting these two paragraphs and accompanying references. They need not be replaced.
Interferon therapy is used (in combination with chemotherapy and radiation) as a treatment for many cancers. This treatment is most effective for treating hematological malignancy; leukemia and lymphomas including hairy cell leukemia, chronic myeloid leukemia, nodular lymphoma, cutaneous T-cell lymphoma. Patients with recurrent melanomas receive recombinant IFN-α2b. Type I IFNs have a therapeutic potential for the treatment of a wide variety of leukemias and solid tumors due to their antiproliferative and apoptotic effects, their anti-angiogenic effects and their ability to modulate an immune response specifically activating dendritic cells, cytolytic T cells and NK cells. Research in this area is receiving intensive investigation.
Comment: This paragraph is misleading. Interferon therapy is not widely “used as a treatment for many cancers”. Reference 21 is not to an article about cancer, perhaps it should have been 22, which, as I mentioned in the previous section, is very old and not appropriate. The rest of the text is also outdated, exaggerated and incorrect. Can be deleted.
Administered intranasally in very low doses, interferon is extensively used in Eastern Europe and Russia as a method to prevent and treat viral respiratory diseases such as cold and flu. However, mechanisms of such action of interferon are not well understood; it is thought that doses must be larger by several orders of magnitude to have any effect on the virus. Although most scientists are skeptical of any claims of good efficacy, recent findings suggest that interferon applied to mucosa may act as an adjuvant against influenza virus, boosting the specific immune system response against the virus. A flu vaccine that uses interferon as adjuvant is currently under clinical trials in the US. Alpha interferon exhibited a significant adjuvant effect in mice, but in a preliminary study it did not exhibit an adjuvant effect for induction of antibody in respiratory secretions of humans to inactivated influenza virus vaccine given intranasally.
A systematic review studied the effect of interferon as a treatment for individuals suffering from herpes simplex virus epithelial keratitis. Topical interferon therapy was shown to be an effective treatment, especially with higher concentrations. Interferon, either used alone or in combination with debridement, appears to be effective as a nucleoside antiviral agent. The combination of interferon and another nucleoside antiviral agent may speed the healing process.
Comment: Interferon is no longer administered intranasally, not even ”in Eastern Europe”. It is not used for herpes simplex virus epithelial keratitis. References 31-37 should be deleted, they are outdated or inappropriate. Need new critical paragraph on currently approved and used therapeutic applications.
It took another fifteen to twenty years, using somatic cell genetics, to show that the interferon action gene and interferon gene reside in different human chromosomes. The purification of human beta interferon did not occur until 1977. Chris Y.H. Tan and his co-workers purified and produced biologically active, radio-labeled human beta interferon by superinducing the interferon gene in fibroblast cells, and they showed its active site contains tyrosine residues. Tan's laboratory isolated sufficient enough amounts of human beta interferon to perform its first amino acid, sugar composition and N-terminal analyses. They showed that human beta interferon was an unusually hydrophobic glycoprotein. This explained a large loss of interferon activity when interferon preparations were transferred from test tube to test tube or from vessel to vessel during purification. The analyses ascertained once and for all, the reality of interferon activity by chemical verification. The purification of human alpha interferon was not reported until 1978. A series of publications from the laboratories of Sidney Pestka and Alan Waldman between 1978 and 1981, describe the purification of the type I interferons IFN-α and IFN-β. By the early 1980s, the genes for these interferons were cloned, allowing for further definitive proof that interferons really were responsible for interfering with viral replication. Gene cloning also confirmed that IFN-α was encoded by, not one gene, but a family of related genes. The type II IFN (IFN-γ) gene was also isolated around this time. Interferon was scarce and expensive until 1980, when the interferon gene was inserted into bacteria using recombinant DNA technology, allowing mass cultivation and purification from bacterial cultures or derived from yeast (e.g. Reiferon Retard is the first yeast derived interferon-alpha 2a) Interferon can also be derived from recombinant mammalian cells. Before this, in the early 1970s the large scale reproduction of human interferon was pioneered by Kari Cantell. He produced large amounts of human alpha interferon from massive quantities of human white blood cells collected from and by the Finnish Blood Bank.Large amounts of human beta interferon were made by superinducing the beta interferon gene in human fibroblast cells, a procedure Chris Y.H.Tan discovered with Monto Ho. Cantell's and Tan's methods of making large amounts of natural interferons were critical to make purified interferons for their chemical characterisation,for their clinical trials and for the preparations of the scarce amount of interferon messenger RNAs to the clone the human alpha and beta interferon genes. The superinduced human beta interferon messenger RNA was prepared by Tan's lab for Cetus corp. to clone the human beta interferon gene into bacteria and the recombinant interferon was developed as 'betaseron' and approved for the treatment of MS. Superinduction of the human beta interferon gene was also used by Israeli scientists to manufacture human beta interferon, used as a topical anti-herpes agent.
Comment: These paragraphs contain numerous factual errors, and there are too many references to the work of Y.H. Tan at the expense of the work of other scientists working in the field. There is advertising to an insignificant product “Reiferon Retard”. The first paragraph refers to work by Sidney Pestka, which is appropriate, but it also mentions Alan Waldman, who was not involved in this work. Some of the wording is overly simplistic (“Interferon was scarce and expensive until 1980, when the interferon gene was inserted into bacteria using recombinant DNA technology, allowing mass cultivation and purification from bacterial cultures”). A complete rewriting of these paragraphs is in order.Kalos01 (talk) 02:45, 18 July 2014 (UTC)