Reevaluation of the Western Equine Encephalitis Antigenic Complex of Alphaviruses (Family Togaviridae) as Determined by Neutralization Tests

Calisher, Charles H.; Karabatsos, Nick; Lazuick, John S.; Monath, Thomas P.; Wolff, K

doi:10.4269/ajtmh.1988.38.447

Cited by 84 publications

(44 citation statements)

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“…In contrast, our MAbs detected a different conserved domain on the NC protein which is absent from VEE and BF viruses. The analysis of epitopes on the NC protein with these antibodies seemed to confirm the relationships between alphaviruses obtained in neutralization tests (Calisher et al, 1980), which reflect similarities only between surface glycoproteins (Trent & Grant, 1980;Calisher et al, 1988). Corresponding relationships have been found by comparison of the amino acid sequences of the glycoproteins of eight alphaviruses ).…”

Section: Discussionmentioning

confidence: 65%

Most Alphaviruses Share a Conserved Epitopic Region on Their Nucleocapsid Protein

Greiser‐Wilke¹,

Moennig²,

Kaaden³

et al. 1989

Journal of General Virology

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SUMMARYFourteen hybridoma cell lines secreting antibodies against the Semliki Forest virus nucleocapsid protein were established and employed for identification of conserved epitopes among 27 alphavirus types and subtypes. Using an antibody capture test, the antibodies were found to cross-react to variable degrees with alphaviruses belonging to the Semliki Forest, western encephalitis and eastern encephalitis complexes, as well as Middelburg and Ndumu. None of the antibodies reacted with either Venezuelan equine encephalitis or Barmah Forest virus. Due to their reactivity with Fort Morgan, Y62-33, Whataroa and chikungunya, the monoclonal antibodies were divided into six reactive types. Competition assays showed that the epitopes for all the types were either identical or clustered on a single domain of the nucleocapsid protein.

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Section: Discussionmentioning

confidence: 65%

Most Alphaviruses Share a Conserved Epitopic Region on Their Nucleocapsid Protein

Greiser‐Wilke¹,

Moennig²,

Kaaden³

et al. 1989

Journal of General Virology

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“…(a) Study organisms (i) The virus BCR virus is a recombinant alphavirus that is part of the western equine encephalitis (WEE)-related virus group (Hayes et al 1977;Calisher et al 1988;Weaver et al 1997). These viruses tend to be vectored by invertebrates (usually mosquitoes) and ampli¢ed and spread over large geographical areas by birds.…”

Section: Methodsmentioning

confidence: 99%

Arbovirus infection increases with group size

Brown

Komar

Quick

et al. 2001

Proc. R. Soc. Lond. B

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Buggy Creek (BCR) virus is an arthropod-borne alphavirus that is naturally transmitted to its vertebrate host the cli¡ swallow (Petrochelidon pyrrhonota) by an invertebrate vector, namely the cimicid swallow bug (Oeciacus vicarius). We examined how the prevalence of the virus varied with the group size of both its vector and host. The study was conducted in southwestern Nebraska where cli¡ swallows breed in colonies ranging from one to 3700 nests and the bug populations at a site vary directly with the cli¡ swallow colony size. The percentage of cli¡ swallow nests containing bugs infected with BCR virus increased signi¢cantly with colony size at a site in the current year and at the site in the previous year. This result could not be explained by di¡erences in the bug sampling methods, date of sampling, sample size of the bugs, age structure of the bugs or the presence of an alternate host, the house sparrow (Passer domesticus). Colony sites that were reused by cli¡ swallows showed a positive autocorrelation in the percentage of nests with infected bugs between year t and year t + 1, but the spatial autocorrelation broke down for year t + 2. The increased prevalence of BCR virus at larger cli¡ swallow colonies probably re£ects the larger bug populations there, which are less likely to decline in size and lead to virus extinction. To the authors' knowledge this is the ¢rst demonstration of arbovirus infection increasing with group size and one of the few known predictive ecological relationships between an arbovirus and its vectors/hosts. The results have implications for both understanding the ¢tness consequences of coloniality for cli¡ swallows and understanding the temporal and spatial variation in arboviral epidemics.

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“…14 To ensure that previous alphavirus vaccination did not affect equine pathogenesis following VEE virus infection, pre-infection equine sera were screened for the presence of VEE, eastern (EEE) and western equine encephalitis (WEE) virus antibodies using three methods: 1) an ELISA with cell lysates prepared from BHK-21 cells infected with VEE virus strain Trinidad donkey, 14 EEE virus strain 82V2137, 15 and WEE virus strain Fleming; 16 2) PRNT using the same virus strains; and 3) hemagglutination inhibition (HI) assays using suckling mouse brain antigens prepared from the same strains.…”

Section: Methodsmentioning

confidence: 99%

Virulence and viremia characteristics of 1992 epizootic subtype IC Venezuelan equine encephalitis viruses and closely related enzootic subtype ID strains.

Wang¹,

Shope²,

Bowen³

et al. 2001

The American Journal of Tropical Medicine and Hygiene

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Abstract. Following a 19-year hiatus, Venezuelan equine encephalitis (VEE) reemerged in western Venezuela in December 1992. This outbreak is important in understanding VEE emergence because phylogenetic studies imply that sympatric, enzootic, subtype ID VEE viruses mutated to generate the epizootic/epidemic. Although the 1992-1993 strains belong to subtype IC, a serotype implicated in extensive outbreaks during the 1960s and in 1995, relatively small numbers of human and equine cases occurred in 1992-1993. We, therefore, evaluated the pathogenicity of these Venezuelan enzootic ID and epizootic IC viruses to determine 1) if they exhibit phenotypes like those described previously for more distantly related enzootic and epizootic strains, and 2) if the 1992-1993 outbreak was limited by the inability of these IC viruses to exploit equines as amplification hosts. All strains were virulent in mice and guinea pigs, but were benign for cotton rats, natural hosts of enzootic viruses. However, only the IC strains produced equine disease, with mean peak viremias of 10 5 suckling mouse 50% lethal doses per mL serum, and some titers exceeding 10 7 . These viremias approximate those observed previously with VEE strains isolated during more extensive epizootics, suggesting that efficient equine amplification did not limit the scope and duration of the 1992-1993 outbreak. Enzootic ID virus infection protected all horses from challenge with epizootic strain P676, supporting the hypothesis that epizootics bypass regions of enzootic transmission due to natural immunization of equines by enzootic VEE viruses.

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Reevaluation of the Western Equine Encephalitis Antigenic Complex of Alphaviruses (Family Togaviridae) as Determined by Neutralization Tests

Cited by 84 publications

References 0 publications

Most Alphaviruses Share a Conserved Epitopic Region on Their Nucleocapsid Protein

Most Alphaviruses Share a Conserved Epitopic Region on Their Nucleocapsid Protein

Arbovirus infection increases with group size

Virulence and viremia characteristics of 1992 epizootic subtype IC Venezuelan equine encephalitis viruses and closely related enzootic subtype ID strains.

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