Introduction: What they say
A study from the Department of Immunology, University of Washington, Seattle, WA 98109, USA; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, WA 98109, USA shows that “RIPK3 Restricts Viral Pathogenesis via Cell Death-Independent Neuroinflammation.” This research paper was published, in the 30 March 2017 issue of the journal “Cell” [One of the best research journals in General biology with an I.F of 28.710], by Prof. Andrew Oberst, Brian P. Daniels and others.
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Antiviral therapy for Neuroinvasive West Nile virus: Ribavirin/Tribavirin, an antiviral drug used in the treatment of RSV infection, hepatitis C, and viral hemorrhagic fever, increases the expression of RIPK3, promotes chemokines production, inhibits neuroinflammation, and restricts neuroinvasive West Nile virus production and pathogenesis in neurons via up regulation of its target gene
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What is known?
Prof. Andrew Oberst’s research team has recently shown that mice deficient in Receptor-interacting protein kinase-3 (RIPK3): a) are highly susceptible to neuroinvasive West Nile virus (WNV); b) poorly induce chemokine expression in neurons; and c) poorly recruit T lymphocytes and inflammatory myeloid cells in central nervous system (CNS).
From Research findings to Therapeutic opportunity:
This study suggests, for the first time, Ribavirin/Tribavirin, used in the treatment of RSV infection, hepatitis C, and viral hemorrhagic fever, may be effective in controlling the production of neuroinvasive West Nile virus (WNV).
Ribavirin/Tribavirin, by increasing the expression of its target gene, it may increase the expression of RIPK3 (Figure 1). Thereby, it may: (1) augment chemokine levels; (2) trigger neuroinflammation; (3) stall neuroinvasive West Nile virus replication; (4) promote clearance of neuroinvasive West Nile virus (WNV); and (5) strengthen antiviral immunity against RNA viruses.
Figure 1 Mechanistic insights into how Ribavirin/Tribavirin functions as an antiviral agent. γ-Bisabolene inhibits neuroinvasive West Nile virus (WNV) pathogenesis via up regulation of its target gene RIPK3
Thus, pharmacological formulations encompassing “Ribavirin/Tribavirin or its analogues, either alone or in combination with any of the known antiviral compounds,” may be used to treat infections caused by neuroinvasive West Nile virus (Figure 1).
Details of the research findings:
Idea Proposed/Formulated (with experimental evidence) by: Dr L Boominathan Ph.D.
Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/
Undisclosed mechanistic information: How does Ribavirin increase the expression of Receptor-interacting protein kinase-3 (RIPK3)?
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# Research cooperation
References:
Web: http://genomediscovery.org or http://newbioideas.com
Citation: Boominathan, L., Antiviral therapy for Neuroinvasive West Nile virus: Ribavirin/Tribavirin, an antiviral drug used in the treatment of RSV infection, hepatitis C, and viral hemorrhagic fever, increases the expression of RIPK3, promotes chemokines production, inhibits neuroinflammation, and restricts neuroinvasive West Nile virus production and pathogenesis in neurons via up regulation of its target gene, 3/November/2017, 7.30 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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