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Expert Opinion on Therapeutic Patents Volume 13, 2003 - Issue 8
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Review

Recent developments in West Nile virus vaccine and antiviral therapy

Anh N Woodmansee Wadsworth Center, New York State Department of Health and Department of Biomedical Sciences, University at Albany, State University of New York, Albany, New York 12201, USA. [email protected]
&
Pei-Yong Shi Wadsworth Center, New York State Department of Health and Department of Biomedical Sciences, University at Albany, State University of New York, Albany, New York 12201, USA. [email protected]
Pages 1113-1125 | Published online: 02 Mar 2005

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  • ••First crystal structure of the MTase domainof NS5 gene for flaviviruses. The structure can serve as the basis for rational design of Inhibitors. In addition, the paper demonstrated, for the first time, the MTase activity of the NS5 protein.
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  • ••First crystal structure of the ectodomain ofthe E protein for flaviviruses.
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  • ••YF 17D vaccine strain as a backbone to make chimera virus for WNV vaccine.
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  • •DEN virus as a backbone to make DEN/WNV chimera for VVNV vaccine development.
  • MANDL CW, HOLZMANN H, MEIXNER T et al.: Spontaneous and engineered deletions in the 3' non-coding region of tick-borne encephalitis virus: construction of highly attenuated mutants of a flavivirus.Virol. (1998) 72:2132–2140.
  • •Attenuation of TBE virus through deletions In the 3'UTR for vaccine development.
  • MANDL CW, ABERLE JH, ABERLE SW et al.: hi vitro-synthesized infectious RNA as an attenuated live vaccine in a flavivirus model. Nat. Med. (1998) 4:1438–1440.
  • DURBIN A, KARRON R, SUN W et al: Attenuation and immunogenicity in humans of a live dengue virus type-4 vaccine candidate with a 30 nucleotide deletion in its 3'-untranslated region. Am. I Trop. Med. Hyg. (2001) 65:405–413.
  • •Attenuation of DEN virus through deletions in the 3'UTR for vaccine development.
  • KOFLER R, HEINZ F, MANDL C: Capsid protein C of tick-borne encephalitis virus tolerates large internal deletions and is a favorable target for attenuation of virulence. J. Viral. (2002) 76:3534–3543.
  • ••First report to describe attenuation of TBEvirus through deletions in the capsid coding region.
  • KOFLER R, LEITNER A, ORIORDAIN G et al.: Spontaneous mutations restore the viability of tick-borne encephalitis virus mutants with large deletions in protein C. Ora (2003) 77:443–451.
  • HALEVY M, AKOV Y, BEN-NATHAN D et al.: Loss of active neuroinvasiveness in attenuated strains of West Nile virus: pathogenicity in immunocompetent and SCID mice. Archiv. Viral. (1994) 137:355–370.
  • LUSTIG S, OLSHEVSKY U, BEN-NATHAN D et al.: A live attenuated West Nile virus strain as a potential veterinary vaccine. Viral Immunol (2000) 13:401–410.
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  • BOROWSKI P, LANG M, HAAG A et al: Characterization of imidazo14,5-dlpyridazine nucleosides as modulators of unwinding reaction mediated by West Nile virus nucleoside triphosphatase/helicase: evidence for activity on the level of substrate and/or enzyme. Antimicrob. Agents Chemother. (2002) 46:1231–1239.
  • ••This paper reported a nucleoside analogue,1-(2'- O-methyl D ribo furanosy6imidazo [4,5- dlpyridazine-4, 7 (5H, 61–4 -dione, as a helicase inhibitor with an EC50 of -30 j.tM in both enzyme and viral infection assays.
  • MORREY J, SMEE D, SIDWELL R et al.: Identification of active antiviral compounds against a New York isolate of West Nile virus. Antiviral Res. (2002) 55:107–116.
  • ••A panel of 34 compounds was tested foranti-WNV activity in a viral infection assay. The compounds 6-azauridine, 6-azauridine triacetate, cyclopententylcytosine, mycophenolic acid, and pyrazofurin showed good antiviral activities.
  • JORDAN I, BRIESE T, FISCHER N et al.: Ribavirin inhibits West Nile virus replication and cytopathic effect in neural cells. J. Infect. Dis. (2000) 182:1214–1217.
  • ••Ribavirin was shown to have anti-WNVactivity in a viral infection assay.
  • CROTTY S, CAMERON CE, ANDINO R: RNA virus error catastrophe: direct molecular test by using ribavirin. Proc. Natl. Acad. Li. USA (2001) 98:6895–6900.
  • GRACI J, CAMERON C: Quasispecies, error catastrophe, and the antiviral activity of ribavirin. Virology (2002) 298:175–180.
  • LEUNG D, SCHRODER K, WHITE H et al.: Activity of recombinant dengue 2 virus N53 protease in the presence of a truncated NS2B co-factor, small peptide substrates, and inhibitors. J. Biol. Chem. (2001) 276:45762–45771.
  • ••Peptic compounds mimicking the conservedcleavage sites (basic residues at the P2 and P1 positions and a residue with a small side chain at the P1' position) with a-keto amide backbones were found to inhibit DEN NS3 protease activity at micromolar concentrations.
  • WU S-F, LEE C-J, LIAO C-L et al.: Antiviral effects of an iminosugar derivative on flavivirus infections. J. Virol (2002) 76:3596–3604.
  • ••ER a-glucosidase inhibitors, which blockthe trimming stem of N-linked glycosylation, were shown to eliminate the production of several ER-budding viruses. One such inhibitor, N-nonyl-deozynojirimycin, was found to inhibit both JE and DEN viruses at micromolar levels.
  • ROEHRIG JT, STAUDINGER LA, HUNT AR et al.: Antibody prophylaxis and therapy for flavivirus encephalitis infections. Ann. NY Acad. Li. (2001) 951:286–297.
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  • SHIMONI Z, NIVEN MJ, PITLICK S: Treatment of West Nile virus encephalitis with intravenous immunoglobulin. Enterg. Infect. Dis. (2001) 7:759.
  • MURTHY HM, JUDGE K, DELUCAS L et al.: Crystal structure of Dengue virus NS3 protease in complex with a Bowman-Birk inhibitor: implications for flaviviral polyprotein processing and drug design. J. Mai Biol. (2000) 301:759–767.
  • ••This paper reported the crystal structure ofNS3 protease domain complexed with a Bowman-Birk inhibitor. Compared with the unliganded NS3, the inhibitor-liganded protease showed a similar overall structure but with significant differences in regions that interact with the inhibitor.
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