ArticleAntiviral research2015
Combined treatment of adenosine nucleoside inhibitor NITD008 and histone deacetylase inhibitor vorinostat represents an immunotherapy strategy to ameliorate West Nile virus infection.
Article in Antiviral research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- Pharmaceutical Strategies for West Nile Virus in Europe, an Underrecognized Cause of Severe Disease and Mortality in Older Adults: From Supportive Care to Antiviral Development.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Drug repurposing: a promising drug discovery strategy for the treatment of emerging epidemic infectious disease.Molecular diversity · 2026Review
- Pathogenicity and virulence of Kyasanur Forest disease: A comprehensive review of an expanding zoonotic threat in southwestern India.Virulence · 2025Review
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- Powassan Virus Induces Structural Changes in Human Neuronal Cells In Vitro and Murine Neurons In Vivo.Pathogens (Basel, Switzerland) · 2022Article
- Pathogenicity and virulence of West Nile virus revisited eight decades after its first isolation.Virulence · 2021Article
- Broad spectrum antiviral nucleosides-Our best hope for the future.Annual reports in medicinal chemistry · 2021Article
- Identification of Zika Virus Inhibitors Using Homology Modeling and Similarity-Based Screening to Target Glycoprotein E.Biochemistry · 2020Article
- The Adenosine Analogue NITD008 has Potent Antiviral Activity against Human and Animal Caliciviruses.Viruses · 2019Article
- Hepatitis E Virus Drug Development.Viruses · 2019Review
- Regulation of Chemokines and Cytokines by Histone Deacetylases and an Update on Histone Decetylase Inhibitors in Human Diseases.International journal of molecular sciences · 2019Review
- Drug repositioning for dengue haemorrhagic fever by integrating multiple omics analyses.Scientific reports · 2019Article
- An "All-In-One" Pharmacophoric Architecture for the Discovery of Potential Broad-Spectrum Anti-Flavivirus Drugs.Applied biochemistry and biotechnology · 2018Article
- Small-Animal Models of Zika Virus.The Journal of infectious diseases · 2017Review
- Minocycline Has Anti-inflammatory Effects and Reduces Cytotoxicity in anJournal of virology · 2017Article
- Zika Virus Infects Human Sertoli Cells and Modulates the Integrity of theJournal of virology · 2017Article
- Pyrrolo[2,3-d]pyrimidine (7-deazapurine) as a privileged scaffold in design of antitumor and antiviral nucleosides.Medicinal research reviews · 2017Review
- Broad-spectrum agents for flaviviral infections: dengue, Zika and beyond.Nature reviews. Drug discovery · 2017Review
- Potential of immunomodulatory agents as adjunct host-directed therapies for multidrug-resistant tuberculosis.BMC medicine · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
West Nile virus (WNV), a member of the Flaviviridae family, is the leading cause of viral encephalitis in the United States. Despite efforts to control the spread of WNV, there has been an increase in the number of outbreaks and clinical cases with neurological problems. There are no antiviral compounds currently in trials for WNV. NITD008 is an adenosine analogue inhibitor that interrupts the RNA-dependent RNA polymerase of flaviviruses. Previous studies demonstrated NITD008 as a potent antiviral for dengue virus, however this drug was associated with preclinical toxicity. The ability of NITD008 to block WNV replication is only shown in Vero cells. Neuroinflammation is also a major cause of the WNV-associated pathology, therefore we evaluated the effect of NITD008 and a newly characterized anti-inflammatory drug vorinostat (SAHA), a histone deacetylase inhibitor, on WNV replication and disease progression in a mouse model. When administered at 10 and 25mg/kg at days 1-6 after WNV infection in C57BL/6 mice, NITD008 conferred complete protection from clinical symptoms and death, which correlated with reduced viral load in the serum and restriction of virus-CNS entry. Delay of NITD008 treatment to days 3-6 and days 5-9 after infection, when WNV replication was high in the periphery and brain, resulted in the gradual loss of protection against WNV infection. However, co-treatment with SAHA and NITD008 during the CNS phase of disease improved disease outcome significantly by reducing inflammation and neuronal death. Our results support potential synergistic effect of combination therapy of NITD008 with SAHA for the treatment of WNV encephalitis.
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