Murray Valley Encephalitis Virus

2020 ◽  
pp. 186-211
Keyword(s):  
Encephalitis Virus ◽  
Murray Valley Encephalitis Virus

scholarly journals The Molecular Epidemiology and Evolution of Murray Valley Encephalitis Virus: Recent Emergence of Distinct Sub-lineages of the Dominant Genotype 1

2015 ◽  
Vol 9 (11) ◽  
pp. e0004240 ◽  
Author(s):  
David T. Williams ◽  
Sinéad M. Diviney ◽  
Aziz-ur-Rahman Niazi ◽  
Peter A. Durr ◽  
Beng Hooi Chua ◽  
...  
Keyword(s):  
Molecular Epidemiology ◽  
Encephalitis Virus ◽  
Genotype 1 ◽  
Murray Valley Encephalitis Virus ◽  
Recent Emergence ◽  
Dominant Genotype

scholarly journals Complete Genome Sequences of the Prototype Isolates of Genotypes 2, 3, and 4 of Murray Valley Encephalitis Virus

2014 ◽  
Vol 2 (3) ◽  
Author(s):  
D. T. Williams ◽  
S. M. Diviney ◽  
K. J. Corscadden ◽  
B. H. Chua ◽  
J. S. Mackenzie
Keyword(s):  
Complete Genome ◽  
Encephalitis Virus ◽  
Murray Valley Encephalitis Virus ◽  
Genome Sequences

Extended detection and isolation of Murray Valley encephalitis virus in whole blood and urine

2019 ◽  
Vol 211 (11) ◽  
pp. 499 ◽  
Author(s):  
Leon Caly ◽  
Natalie Davidson ◽  
Ram Ghimire ◽  
Brinthan Rajaratnam ◽  
Jonathan Marrow ◽  
...  
Keyword(s):  
Whole Blood ◽  
Encephalitis Virus ◽  
Murray Valley Encephalitis Virus

Opportunistic serological surveillance for Murray Valley encephalitis virus in Victoria, February–May 2011

2012 ◽  
Vol 197 (3) ◽  
pp. 150-150 ◽  
Author(s):  
Joseph S Doyle ◽  
Suellen Nicholson ◽  
Jennifer A Leydon ◽  
Rodney J Moran ◽  
Michael G Catton
Keyword(s):  
Encephalitis Virus ◽  
Murray Valley Encephalitis Virus ◽  
Serological Surveillance

Murray Valley Encephalitis Virus

2004 ◽  
pp. 860-864
Author(s):  
David W. Smith ◽  
Annette K. Broom ◽  
John S. Mackenzie
Keyword(s):  
Encephalitis Virus ◽  
Murray Valley Encephalitis Virus

scholarly journals Live Chimeric and Inactivated Japanese Encephalitis Virus Vaccines Differ in Their Cross-Protective Values against Murray Valley Encephalitis Virus

2008 ◽  
Vol 83 (6) ◽  
pp. 2436-2445 ◽  
Author(s):  
Mario Lobigs ◽  
Maximilian Larena ◽  
Mohammed Alsharifi ◽  
Eva Lee ◽  
Megan Pavy
Keyword(s):  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Protective Immunity ◽  
Encephalitis Virus ◽  
Type I ◽  
Murray Valley Encephalitis Virus ◽  
Lethal Challenge ◽  
Live Virus ◽  
Immunodeficient Mice ◽  
The Cross

ABSTRACT The Japanese encephalitis virus (JEV) serocomplex, which also includes Murray Valley encephalitis virus (MVEV), is a group of antigenically closely related, mosquito-borne flaviviruses that are responsible for severe encephalitic disease in humans. While vaccines against the prominent members of this serocomplex are available or under development, it is unlikely that they will be produced specifically against those viruses which cause less-frequent disease, such as MVEV. Here we have evaluated the cross-protective values of an inactivated JEV vaccine (JE-VAX) and a live chimeric JEV vaccine (ChimeriVax-JE) against MVEV in two mouse models of flaviviral encephalitis. We show that (i) a three-dose vaccination schedule with JE-VAX provides cross-protective immunity, albeit only partial in the more severe challenge model; (ii) a single dose of ChimeriVax-JE gives complete protection in both challenge models; (iii) the cross-protective immunity elicited with ChimeriVax-JE is durable (≥5 months) and broad (also giving protection against West Nile virus); (iv) humoral and cellular immunities elicited with ChimeriVax-JE contribute to protection against lethal challenge with MVEV; (v) ChimeriVax-JE remains fully attenuated in immunodeficient mice lacking type I and type II interferon responses; and (vi) immunization with JE-VAX, but not ChimeriVax-JE, can prime heterologous infection enhancement in recipients of vaccination on a low-dose schedule, designed to mimic vaccine failure or waning of vaccine-induced immunity. Our results suggest that the live chimeric JEV vaccine will protect against other viruses belonging to the JEV serocomplex, consistent with the observation of cross-protection following live virus infections.

scholarly journals Attenuation of Murray Valley Encephalitis Virus by Site-Directed Mutagenesis of the Hinge and Putative Receptor-Binding Regions of the Envelope Protein

2001 ◽  
Vol 75 (16) ◽  
pp. 7692-7702 ◽  
Author(s):  
Robert J. Hurrelbrink ◽  
Peter C. McMinn
Keyword(s):  
Amino Acid ◽  
Receptor Binding ◽  
Encephalitis Virus ◽  
Hinge Region ◽  
Wild Type Virus ◽  
Binding Motif ◽  
Murray Valley Encephalitis Virus ◽  
Ligand Interaction

ABSTRACT Molecular determinants of virulence in flaviviruses cluster in two regions on the three-dimensional structure of the envelope (E) protein; the base of domain II, believed to serve as a hinge during pH-dependent conformational change in the endosome, and the lateral face of domain III, which contains an integrin-binding motif Arg-Gly-Asp (RGD) in mosquito-borne flaviviruses and is believed to form the receptor-binding site of the protein. In an effort to better understand the nature of attenuation caused by mutations in these two regions, a full-length infectious cDNA clone of Murray Valley encephalitis virus prototype strain 1-51 (MVE-1-51) was employed to produce a panel of site-directed mutants with substitutions at amino acid positions 277 (E-277; hinge region) or 390 (E-390; RGD motif). Viruses with mutations at E-277 (Ser→Ile, Ser→Asn, Ser→Val, and Ser→Pro) showed various levels of in vitro and in vivo attenuation dependent on the level of hydrophobicity of the substituted amino acid. Altered hemagglutination activity observed for these viruses suggests that mutations in the hinge region may indirectly disrupt the receptor-ligand interaction, possibly by causing premature release of the virion from the endosomal membrane prior to fusion. Similarly, viruses with mutations at E-390 (Asp→Asn, Asp→Glu, and Asp→Tyr) were also attenuated in vitro and in vivo; however, the absorption and penetration rates of these viruses were similar to those of wild-type virus. This, coupled with the fact that E-390 mutant viruses were only moderately inhibited by soluble heparin, suggests that RGD-dependent integrin binding is not essential for entry of MVE and that multiple and/or alternate receptors may be involved in cell entry.

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