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Antiviral therapy against Neuroinvasive West Nile virus: Nimodipine, an anti-hypertensive agent, 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, 7/January/2017, 10.38 pm

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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 OberstBrian 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 against Neuroinvasive West Nile virus: Nimodipine, an anti-hypertensive agent, 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

Price 300[easy_payment currency=”USD”]


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, that the anti-hypertensive medication Nimodipine may aid in attenuating the replication of  RNA viruses such as neuroinvasive West Nile virus (WNV).

Nimodipine, 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 Nimodipine may function as an anti-viral agent. Nimodipine inhibits neuroinvasive West Nile virus (WNV) pathogenesis via up regulation of its target gene RIPK3

Figure 2. The chemical structure of Nimodipine.

Thus, pharmacological formulations encompassing Nimodipine 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 (Figures 1-2 ).


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 Nimodipine increase the expression of Receptor-interacting protein kinase-3 (RIPK3)?

Amount: $300#

For payment and purchase details, you may reach us at admin@genomediscovery.org

# Research cooperation


References:

Web: http://genomediscovery.org or http://newbioideas.com

Citation: Boominathan, L., Antiviral therapy against Neuroinvasive West Nile virus: Nimodipine, an anti-hypertensive agent, 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, 7/January/2017, 10.37 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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