J Gen Virol. Nucleotide changes responsible for loss of neuroinvasiveness in Japanese encephalitis virus neutralization-resistant mutants. Inhibition of West Nile virus entry by using a recombinant domain III from the envelope glycoprotein.
Monoclonal antibodies that bind to domain III of dengue virus E glycoprotein are the most efficient blockers of virus adsorption to Vero cells. Journal of Molecular Graphics. Phylogenetic relationships of flaviviruses correlate with their epidemiology, disease association and biogeography. Humanized monoclonal antibodies derived from chimpanzee Fabs protect against Japanese encephalitis virus in vitro and in vivo.
Flavivirus structure and membrane fusion. Adv Virus Res. Characterization of monoclonal antibody-escape mutants of tick-borne encephalitis virus with reduced neuroinvasiveness in mice. An external loop region of domain III of dengue virus type 2 envelope protein is involved in serotype-specific binding to mosquito but not mammalian cells.
Crystal structure of west nile virus envelope glycoprotein reveals viral surface epitopes. J Mol Graph. Structure of dengue virus: implications for flavivirus organization, maturation, and fusion. Biological transmission of arboviruses: reexamination of and new insights into components, mechanisms, and unique traits as well as their evolutionary trends.
Clin Microbiol Rev. Phylogeny of the genus Flavivirus. A functional epitope determinant on domain III of the Japanese encephalitis virus envelope protein interacted with neutralizing-antibody combining sites. Antigenic structure of the flavivirus envelope protein E at the molecular level, using tick-borne encephalitis virus as a model. A ligand-binding pocket in the dengue virus envelope glycoprotein. Variable surface epitopes in the crystal structure of dengue virus type 3 envelope glycoprotein.
NMR solution structure and backbone dynamics of domain III of the E protein of tick-borne Langat flavivirus suggests a potential site for molecular recognition. Protein Sci. Structure of West Nile virus. Crystal structure of dengue virus type 1 envelope protein in the postfusion conformation and its implications for membrane fusion.
Crystal structure of the West Nile virus envelope glycoprotein. Structural basis of West Nile virus neutralization by a therapeutic antibody. The envelope glycoprotein from tick-borne encephalitis virus at 2 A resolution. Monoclonal antibody mapping of the envelope glycoprotein of the dengue 2 virus. Mutation in a 17D vaccine substrain-specific envelope protein epitope alters the pathogenesis of yellow fever virus in mice.
Characterization of neutralizing antibodies to West Nile virus. Type- and subcomplex-specific neutralizing antibodies against domain III of dengue virus type 2 envelope protein recognized adjacent epitopes.
J Biol Chem. Structure of the envelope protein domain III of Omsk hemorrhagic fever virus. NMR Assign. Solution structure of the envelope protein domain III of dengue-4 virus. Japanese encephalitis virus antigenic variants with characteristic differences in neutralization resistance and mouse virulence. Virus Res. David E. Volk, Fiona J. May, Sai H. Gandham, Anjenique Anderson, Jana J. Von Lindern, David W. Beasley , Alan D. Yellow fever virus YFV is the prototype member of the genus Flavivirus , which contains more than 60 positive-sense, single-stranded RNA viruses, many of which are considered public health threats.
YF disease is controlled by a live attenuated vaccine, 17D, which was generated empirically through serial passage of the wild-type WT strain Asibi in chicken tissue. The vaccine, which has been used for over 80 years, is considered to be one of the safest and most effective live attenuated vaccines. Twitter Facebook. Yellow Fever Virus 1. Introduction Yellow fever is an acute viral hemorrhagic disease caused by yellow fever virus YFV , a prototype of the Genus Flavivirus of the family Flaviviridae.
Occasionally humans working or travelling in the forest are bitten by infected mosquitoes and develop yellow fever. Increased contact between people and infected mosquitoes leads to increased transmission and many separate villages in an area can develop outbreaks at the same time. This is the most common type of outbreak in Africa. In these conditions, infected mosquitoes transmit the virus from person to person. Transmission cycles of yellow fever. Signs and Symptoms The incubation period is 3—6 days.
Figure 2. Major symptom of yellow fever. The virus may be recovered from the blood the first 4 days after onset or from postmortem tissue by intracerebral inoculation of mice or by use of cell lines. Serology IgM antibodies appear during the first week of illness. The detection of IgM antibody by ELISA capture in a single sample provides a presumptive diagnosis, with confirmation by a fourfold or greater rise in titer of neutralizing antibody between acute phase and convalescent phase serum samples.
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