Headline in the journal Science:
“Can the interferons help the body beat COVID-19?”
Interferon is the foot soldier of our immune system, the “interfering particle” recruited by the appearance of an enemy pathogen. Interferon is a protein capable of incapacitating an enemy virus as well as warning neighboring cells to arm themselves against infection, commanding a Masada-like mass suicide of cells or calling in a predator strike from more powerful, special forces in the immune system.
— from Isaacs to Silver. Interferon and the MPNs
There’s a deep irony and an MPN connection to this breakthrough Science story. Call it the Jeremy Effect.
The Science 
story opens in the Stanford University Medical Center with Patient 16 getting an injection of either placebo or interferon in a clinical trial.;
We know Stanford as the epicenter of Western resistance to interferon use in treating myeloproliferative neoplasm.
Jeremy Smith’s personal physician to manage his polycythemia vera was the late Dr. Stanley Schrier. a former president of ASH and long-term hematology division chief at Stanford. Pending results of a double blind randomized clinical trial he led the refusal to endorse the interferons despite strong anecdotal evidence.
Fighting stiff resistance, once Jeremy Smith’s PV progressed to myelofibrosis he insisted on interferon treatment to replace hydroxyurea. He submitted copies of papers, articles from MPNforum, testimony from Dr. Hans Hasselbalch, Dr. Silver and others to support his request. And he persevered. Reluctantly , Jeremy Smith was put on interferon and almost immediately he started showing dramatic results.
Today. Jeremy is celebrating his 31st year living his life with an MPN and the interferon he fought so hard for to get has kept his numbers stable after transitioning to Myelofibrosis in 2012. Jeremy says after finally getting off Hydrea and on to interferon the brain fog that MPN patients often complain about was gone and his energy completely returned and he left days of fatigue behind.
Any chance the interferons can repeat that kind of performance against SARS-coV-2, the virus causing COVID-19? It’s a lot more than just promising.
“.. a small flurry of recent papers,” writes Meredith Wadman, Science writer, “suggest the novel coronvirus s does some of its deadly work by disabling interferons, powerful proteins that are the body’s own front-line defenders against viral invasion,. If so, synthetic interferons given before or soon after infection may tame the virus before it causes serious disease…” The Stanford trial is one of dozens testing interferon efficacy with people who might have been exposed to the virus, Wadman reports: “Every study in every species has shown that if you induce interferons before virus comes in, the virus loses says Andreas Wack, an immunologist at the Francis Crick Institute. The earlier you can give it, the better…”
That observation was underscored by a note we received from Dr. Richard T. Silver July 13:
“Perhaps your readers would like to know that two familiar drugs, ruxlolitinib and interferon are being evaluated in COVID. Rux, because of its anti-inflammatory properties, and interferon because it is antiviral agent. It is our feeling both drugs should be used early in the course of the disease. Definite answers pending.”
The anecdotal evidence for interferon’s effectiveness is impresssive. “In an early unrandomized preventive trial in a hospital in China’s Hubei province,”writes Wadman, “none of the 2415 medical workers who took daily interferon nose drops got the virus…”
University of Toronto immunologist., Eleanor Fish, reported an uncontrolled 77 patient trial in Wuhan , China i
n Frontiers in Immunology. Those patients given a Type I interferon showed lower levels of a a critical inflammatory biomarker thaand cleared the virus a ful week earlier than other patients.
“The result,” write Fish and her associates, ” indicate that an IFN-α RCT [randomized control trial] is now warranted. Furthermore, since the entire cohort consisted only of moderate cases of COVID-19 disease, our findings may not be indicative of what occurs in more severely ill patients; such caution about generalizability is indeed further supported by the limited impact of age, sex and comorbidities on the course of COVID-19 disease in our cohort, as each of these have been shown to have varying degrees of influence on clinical course.
“Irrespective of these significant limitations, to our knowledge, the findings presented here are the first to suggest therapeutic efficacy in COVID-19 disease of IFN-α2b, an available antiviral intervention. Furthermore, beyond clinical benefit to the individual patient, treatment with IFN-α2b may also benefit public health measures aimed at slowing the tide of this pandemic, in that duration of viral shedding appears shortened.”
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