Antiviral therapy against Hepatitis-B virus: Gatifloxacin, an antibiotic drug,  increases the expression of Setd2, methylates STAT1, activates STAT1, promotes trimethylation of IFN-stimulated gene-15, and restricts Hepatitis-B virus (HBV) production and pathogenesis via up regulation of its target gene, 15/October/2017,  12.38 am

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Introduction: What they say

A study from the Institute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China; and Institute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China; National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai 200433, China; Department of Immunology & Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China shows that “Methyltransferase SETD2-Mediated Methylation of STAT1 Is Critical for Interferon Antiviral Activity.” This research paper was published, in the 27 July 2017 issue of the journal “Cell” [One of the best research journals in General biology with an I.F of 28.710], by Prof. Cao X, Chen K 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 Hepatitis-B virus: Gatifloxacin, an antibiotic drug,  increases the expression of Setd2, methylates STAT1, activates STAT1, promotes trimethylation of IFN-stimulated gene-15, and restricts Hepatitis-B virus (HBV) production and pathogenesis via up regulation of its target gene


From Significance of the study to Public health relevance:

Given that: (1) nearly 2.5 billion (~1/3) people out of 7.4 billion total world population are infected with Hepatitis virus; (2) nearly 343 million people are chronically infected with Hepatitis virus; (3) over 750,000 people lose their life for hepatitis each year; and nearly half of them die due to liver cancer; (4) molecular pathways involved and the mechanism of development of drug-resistant Hepatitis-B virus is far from understood; (4) treating drug-resistant Hepatitis-B virus is still a daunting task; (5) nearly 129 million new infections occurred in 2013; (6) newborns who acquired Hepatitis-B virus (HBV) from mothers face 40% lifetime risk of death either due to cirrhosis or hepatocellular carcinoma; (7) billions of dollars are being spent each year globally for the treatment of Hepatitis virus; and (8) most of the Hepatitis-B virus cases are registered in developing countries, such as East Asia and sub-Saharan Africa—that cannot afford high-cost treatment required for drug-resistant Hepatitis-B virus—compared to developed countries, such as US and UK, there is an urgent need to find: (i) a way to inhibit drug-resistant Hepatitis-B virus; (ii) a cheaper alternative to the existing expensive drugs; and (iii) a side-effect-free-Natural product-based drug that prevents relapse/recurrence of drug-resistant Hepatitis-B virus.


What is known?

Prof. Cao X’s research team has recently shown that Setd2: a) conditional null mice (Setd2 was deleted only in hepatocytes) are highly susceptible to Hepatitis-B virus (HBV) infection; b) methylates Signal transducers and activators of transcription 1 (STAT1) at lysine 525; c) reinforces Interferon (IFN)-activated STAT1 phosphorylation; d) catalyzes trimethylation of H3K36 on promoters of IFN-stimulated genes, including IFN-stimulated gene-15; and e) promotes IFNa-mediated antiviral immunity, suggesting that increasing the expression of SETD2 may promote IFNα-dependent antiviral immunity and control viral infections, including infections caused by HBV.


From Research findings to Therapeutic opportunity:

This study suggests, for the first time, a natural product-based antiviral therapy against infections caused by HBV.

Gatifloxacin, by increasing the expression of its target gene, it may increase the expression of Setd2 (Figure 1). Thereby, it may: (1) methylate STAT1 at lysine 525; (2) promote IFN-mediated STAT1 phosphorylation; (3) activate STAT1; (4) trimethylate H3K36 on promoters of IFN-stimulated genes, such as IFN-stimulated gene-15; (5) increase the expression of antimicrobial peptides; (6) augment IFN-α-mediated antiviral immunity; (7) stall Hepatitis-B virus (HBV) replication; (8) inhibit liver damage; (9) promote clearance of HBV; and (10) strengthen antiviral immunity against RNA viruses. Thus, pharmacological formulations encompassingGatifloxacin or its analogues, either alone or in combination with other antiviral drugs” may be used to treat infections caused by RNA viruses such as HBV (Figure 1).

Figure 1 Gatifloxacin as an an anti-Hepatitis-B virus (HBV) agent. Gatifloxacin inhibits infections caused by RNA viruses such as HBV via up regulation of its target gene Setd2

 


Details of the research findings:

Idea Proposed/Formulated (with experimental evidence) by: Dr L Boominathan Ph.D.

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Undisclosed mechanistic information: How does Gatifloxacin increase the expression of methyl transferase Setd2, FN-stimulated gene-15 and antimicrobial peptides?

Amount: $500#

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References:

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

Citation: Boominathan, L., Antiviral therapy against Hepatitis-B virus: Gatifloxacin, an antibiotic drug,  increases the expression of Setd2, methylates STAT1, activates STAT1, promotes trimethylation of IFN-stimulated gene-15, and restricts Hepatitis-B virus (HBV) production and pathogenesis via up regulation of its target gene, 15/October/2017,  12.38 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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