The Japanese Encephalitis Serological Group of Flaviviruses: a Brief Introduction to the Group

Mackenzie, John S.; Barrett, Alan D.T.; Denis, Vincent

doi:10.1007/978-3-642-59403-8_1

Cited by 74 publications

(75 citation statements)

References 25 publications

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“…It is the leading cause of viral encephalitis in humans worldwide, and it is responsible for more than 30,000 cases of human disease each year and up to 25% mortality, many of those in children under 12 years old. [2][3][4] JEV is also a significant pathogen of horses, causing death from encephalitis in as many as 40% of clinical cases. 2 The endemic cycle of JEV allows it to circulate between ardeid birds, culicine mosquitoes, and domestic pigs, but during epidemic years, the spillover into humans and horses can have disastrous consequences.…”

Section: Introductionmentioning

confidence: 99%

Pathogenesis of Japanese Encephalitis Virus Infection in a Golden Hamster Model and Evaluation of Flavivirus Cross-Protective Immunity

Bosco‐Lauth

Mason²,

Bowen³

2011

The American Society of Tropical Medicine and Hygiene

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Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus endemic to Southeast Asia and surrounding Pacific Islands, and it has most recently emerged in northern Australia. JEV is closely related to West Nile virus (WNV) and St. Louis encephalitis virus (SLEV), both endemic to the United States. In the event that JEV is introduced into the Americas, it will be important to determine whether immunity to WNV or SLEV might afford protection from infection and development of viremia in susceptible hosts. We investigated a hamster model of JEV infection and showed that a large fraction of animals infected with either a genotype I or III isolate of virus developed viremia and encephalitic lesions without clinical signs of disease. Using this model, we showed that prior infection with WNV or SLEV, vaccination using a chimeric WNV vaccine, and passive immunization with anti-JEV immune sera prevented viremia in hamsters challenged with JEV.

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Section: Introductionmentioning

confidence: 99%

Pathogenesis of Japanese Encephalitis Virus Infection in a Golden Hamster Model and Evaluation of Flavivirus Cross-Protective Immunity

Bosco‐Lauth

Mason²,

Bowen³

2011

The American Society of Tropical Medicine and Hygiene

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“…These viruses are mosquito borne, primarily transmitted by Culex spp., and have wide, overlapping distributions throughout the world (22).…”

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confidence: 99%

Envelope Protein Glycosylation Status Influences Mouse Neuroinvasion Phenotype of Genetic Lineage 1 West Nile Virus Strains

Beasley

Whiteman

Zhang

et al. 2005

J Virol

285

261

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The introduction of West Nile virus (WNV) into. To begin to elucidate the basis for these differences, we compared a highly virulent New York 1999 (NY99) isolate with a related Old World lineage 1 strain, An4766 (ETH76a), which is attenuated for mouse neuroinvasion. Genomic sequencing of ETH76a revealed a relatively small number of nucleotide (5.1%) and amino acid (0.6%) differences compared with NY99. These differences were located throughout the genome and included five amino acid differences in the envelope protein gene. Substitution of premembrane and envelope genes of ETH76a into a NY99 infectious clone backbone yielded a virus with altered in vitro growth characteristics and a mouse virulence phenotype comparable to ETH76a. Further site-specific mutagenesis studies revealed that the altered phenotype was primarily mediated via loss of envelope protein glycosylation and that this was associated with altered stability of the virion at mildly acidic pH. Therefore, the enhanced virulence of North American WNV strains compared with other Old World lineage 1 strains is at least partly mediated by envelope protein glycosylation.

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“…However, the long persistence of WNV antibodies in birds (McIntosh et al, 1969;Gibbs et al, 2005;Wilcox et al, 2007), and the fact that no parallel testing was done to rule out crossreactive flaviviruses as the causative infection (blood sample volumes were kept to a minimum to avoid survival risks to the studied birds), both prevent a formal identification of the virus responsible for the detected antibodies. Other possible viruses include those from the Japanese encephalitis (e.g., Yaounde virus, Usutu virus) or the Yellow fever (e.g., Uganda S virus) serologic groups, viruses which have occasionally been isolated from birds in sub-Saharan Africa (Mackenzie et al, 2002;Simpson, 1993). Usutu virus is considered to be established in Central Europe (Chvala et al, 2007;Meister et al, 2008).…”

mentioning

confidence: 99%

Prevalence of West Nile Virus Neutralizing Antibodies in Wild Birds from the Camargue Area, Southern France

Jourdain

Zeller

Sabatier³

et al. 2008

Journal of Wildlife Diseases

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The Japanese Encephalitis Serological Group of Flaviviruses: a Brief Introduction to the Group

Cited by 74 publications

References 25 publications

Pathogenesis of Japanese Encephalitis Virus Infection in a Golden Hamster Model and Evaluation of Flavivirus Cross-Protective Immunity

Pathogenesis of Japanese Encephalitis Virus Infection in a Golden Hamster Model and Evaluation of Flavivirus Cross-Protective Immunity

Envelope Protein Glycosylation Status Influences Mouse Neuroinvasion Phenotype of Genetic Lineage 1 West Nile Virus Strains

Prevalence of West Nile Virus Neutralizing Antibodies in Wild Birds from the Camargue Area, Southern France

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