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Anti-infective Therapy: Fluvastatin, a lipid-lowering drug used in the treatment of hypercholesterolemia and cardiovascular disease, inhibits Hepatitis-B/C, Dengue, Zika, Ebola, HIV-1, Mtb, Malaria, CMV, Influenza H1NI1,  respiratory syncytial,  Sindbis, and SFV viruses by increasing the Levels of the Antiviral Proteins IFITM3, & Interferon-stimulated gene 15, 10/January/2017,  11.11 pm

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Introduction: What they say:

A study from the Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard Medical School, Charlestown, MA 02129, USA shows that “The IFITM proteins mediate cellular resistance to influenza A H1N1 virus, West Nile virus, and dengue virus.” This study was published, in the 24 December 2009 issue of the journal “Cell” (the number 1 research journal in General Biology with an impact factor of 33),  by the 2015 Laskar award winner Prof. Stephen Elledge, Brass and others.


What we say: 

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that:   Anti-infective Therapy: Fluvastatin, a lipid-lowering drug used in the treatment of hypercholesterolemia and cardiovascular disease, inhibits Hepatitis-B/C, Dengue, Zika, Ebola, HIV-1, Mtb, Malaria, CMV, Influenza H1NI1,  respiratory syncytial,  Sindbis, and SFV viruses by increasing the Levels of the Antiviral Proteins IFITM3, & Interferon-stimulated gene 15


What is known?

Prof. Stephen Elledge research team has showed that interferon-inducible transmembrane proteins IFITM1, 2, and 3 inhibit  influenza A H1N1 virus, West Nile virus, and dengue virus replication, suggesting that increasing the expression of IFITM3 may confer resistance against these viruses. Other studies suggest that IFITM3 may also protect against Ebola virus, hepatitis C virus, yellow fever virus and SARS coronavirus etc.


From research findings to therapeutic opportunity: 

This study suggests, for the first time, that Fluvastatin, by increasing the expression of its target genes, it may increase the expression of interferon-inducible transmembrane protein IFITM3, Interferon-stimulated gene-15, Mx2 and antimicrobial peptides. Thereby, it may: (1) inhibit the replication of  Hepatitis-B/C, Dengue, Zika, Ebola, HIV-1, Mtb, Malaria, CMV, Influenza H1NI1,  respiratory syncytial,  Sindbis, and SFV viruses; (2) confer resistance against  infection caused by Hepatitis-B/C, Dengue, Zika, Ebola, HIV-1, Mtb, Malaria, CMV, Influenza H1NI1,  respiratory syncytical,  Sindbis, and SFV viruses; and (3) promote innate immunity (Figure 1) Thus, pharmacological formulations encompassing “Fluvastatin or its analogues, either alone or in combination with other drugs” may be used to prevent/treat infections caused by Hepatitis-B/C, Dengue, Zika, Ebola, HIV-1, Mtb, Malaria, CMV, Influenza H1NI1,  respiratory syncytial,  Sindbis, and SFV viruses (Figure 2).

Figure 1. Mechanistic insight into how Fluvastatin  inhibits Hepatitis-B/C, Dengue, Zika, Ebola, HIV-1, Mtb, Malaria, CMV, Influenza H1NI1,  respiratory syncytial , Sindbis, and SFV viruses production through induction of its target genes, such as antiviral Proteins IFITM3, Interferon-stimulated gene 15, & Mx2

Figure 2. The chemical structure of Fluvastatin. Fluvastatin may function as a broad-spectrum anti-infective agent


Details of the research findings: 

Idea formulated by Dr L Boominathan PhD

Undisclosed information: How Fluvastatin increases the expression of Antiviral Protein IFITM3, , Interferon-stimulated gene 15, & Mx2

Amount: $ 500#

# Research cooperation

For more details on payment, you may reach us at admin@genomediscovery.org


References: 

CitationBoominathan L, Anti-infective Therapy: Fluvastatin, a lipid-lowering drug used in the treatment of hypercholesterolemia and cardiovascular disease, inhibits Hepatitis-B/C, Dengue, Zika, Ebola, HIV-1, Mtb, Malaria, CMV, Influenza H1NI1,  respiratory syncytial,  Sindbis, and SFV viruses by increasing the Levels of the Antiviral Proteins IFITM3, & Interferon-stimulated gene 15, 10/January/2017,  11.11 pm
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