Enzootic and Epizootic Venezuelan Equine Encephalomyelitis Virus in Horses Infected by Peripheral and Intrathecal Routes

Dietz, William H.; Alvarez, Otto; Martín, David H.; Walton, T. E.; Ackerman, Larry J.; Johnson, Karl M.

doi:10.1093/infdis/137.3.227

Cited by 22 publications

(20 citation statements)

References 13 publications

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“…2,7,8,[24][25][26][27][28] Equine mortality rates in these previous studies were generally approximately 50%, similar to those measured during epizootics. In contrast, enzootic VEE viruses belonging to subtypes ID, 7 IE, 29 II, 24 III, and IV 30 generally produce little or no clinical illness and viremia less than 10 5 SMicLD 50 / mL serum following experimental equine infection.…”

Section: Discussionmentioning

confidence: 53%

“…5,6 Venezuelan equine encephalitis virus strains implicated in most outbreaks belong to antigenic subtypes IAB and IC, while all other members of the VEE antigenic complex are considered enzootic viruses that circulate continuously, are generally avirulent for equines, and are incapable of epizootic amplification due to their inability to generate sufficient viremia in horses, donkeys, and mules. 1,7,8 The discontinuous nature of VEE outbreaks resulted in many years of research to identify a source of the subtype IAB and IC viruses implicated in epidemics and epizootics. Although some outbreaks prior to 1980 may have been initiated by the use of incompletely inactivated vaccines made from virulent, epizootic IAB viruses, 9 the original evolutionary source of the IAB and IC viruses is believed to be enzootic, subtype ID viruses that circulate in northern South America.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 53%

Section: Introductionmentioning

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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“…The latter strain is often used as an enzootic control in experimentation and is considered avirulent in horses on the basis of its close genetic relatedness to strains that have been experimentally evaluated in horses. 22,23 All four viruses were detected in the saliva of mosquitoes that imbibed low-titer blood meals. Some variability existed between and within groups, although the level and degree did not differ from that seen previously with experimental infection of Cx.…”

Section: Discussionmentioning

confidence: 99%

Vector Competence of Culex (Melanoconion) taeniopus for Equine-Virulent Subtype IE Strains of Venezuelan Equine Encephalitis Virus

Deardorff¹,

Weaver

2010

The American Society of Tropical Medicine and Hygiene

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Abstract. The mosquito Culex ( Melanoconion ) taeniopus is a proven vector of enzootic Venezuelan equine encephalitis virus (VEEV) subtype IE in Central America. It has been shown to be highly susceptible to infection by this subtype, and conversely to be highly refractory to infection by other VEEV subtypes. During the 1990s in southern coastal Mexico, two VEE epizootics in horses were attributed to subtype IE VEEV. These outbreaks were associated with VEEV strains with an altered infection phenotype for the epizootic mosquito vector, Aedes ( Ochlerotatus ) taeniorhynchus. To determine the infectivity for the enzootic vector, Culex taeniopus, mosquitoes from a recently established colony were orally exposed to VEEV strains from the outbreak. The equine-virulent strains exhibited high infectivity and transmission potential comparable to a traditional enzootic subtype IE VEEV strain. Thus, subtype IE VEEV strains in Chiapas are able to efficiently infect enzootic and epizootic vectors and cause morbidity and mortality in horses.

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“…Although humans can develop severe and sometime fatal disease from infection with VEE subtype IE viruses when they contact sylvatic transmission foci, they are believed to be only tangential hosts that do not serve as a reservoir to infect mosquitoes. Experimental infections of previous enzootic IE strains indicated that they are generally equine avirulent and produce little or no viremia in equines (9,11,42,43). The two Mexican outbreaks of equine encephalitis mark the first isolations of subtype IE VEEV from equines and the first confirmed cases of equine disease as a result of VEEV subtype IE infection (27).…”

mentioning

confidence: 99%

Positively Charged Amino Acid Substitutions in the E2 Envelope Glycoprotein Are Associated with the Emergence of Venezuelan Equine Encephalitis Virus

Brault

Powers

Holmes

et al. 2002

J Virol

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Epidemic-epizootic Venezuelan equine encephalitis (VEE) viruses (VEEV) have emerged repeatedly via convergent evolution from enzootic predecessors. However, previous sequence analyses have failed to identify common sets of nucleotide or amino acid substitutions associated with all emergence events. During 1993 and 1996, VEEV subtype IE epizootics occurred on the Pacific Coast of the states of Chiapas and Oaxaca in southern Mexico. Like other epizootic VEEV strains, when inoculated into guinea pigs and mice, the Mexican isolates were no more virulent than closely related enzootic strains, complicating genetic studies of VEE emergence. Complete genomic sequences of 4 of the Mexican strains were determined and compared to those of closely related enzootic subtype IE isolates from Guatemala. The epizootic viruses were less than 2% different at the nucleotide sequence level, and phylogenetic relationships confirmed that the equine-virulent Mexican strains probably evolved from enzootic progenitors on the Pacific Coast of Mexico or Guatemala. Of 35 amino acids that varied among the Guatemalan and Mexican isolates, only 8 were predicted phylogenetically to have accompanied the phenotypic change. One mutation at position 117 of the E2 envelope glycoprotein, involving replacement of Glu by Lys, resulted in a small-plaque phenotype characteristic of epizootic VEEV strains. Analysis of additional E2 sequences from representative enzootic and epizootic VEEV isolates implicated similar surface charge changes in the emergence of previous South American epizootic phenotypes, indicating that E2 mutations are probably important determinants of the equine-virulent phenotype and of VEE emergence. Maximum-likelihood analysis indicated that one change at E2 position 213 has been influenced by positive selection and convergent evolution of the epizootic phenotype.Venezuelan equine encephalitis virus (VEEV) is a member of the family Togaviridae in the genus Alphavirus (14, 48). The virus is enveloped and includes a nonsegmented, positive-sense RNA genome of approximately 11.5 kb. The 5' two-thirds of the genome encodes four nonstructural proteins (nsP1 to 4) that are involved in viral replication. After virus entry into the cytoplasm of cells, a nonstructural polyprotein is translated and utilized in the production of full-length negative-sense RNA. The negative-sense RNA is used for the generation of genomic RNA as well as a subgenomic mRNA (26S) that is homologous to the 3' one-third of the genome. The subgenomic RNA is translated directly into a structural polyprotein that is proteolytically cleaved into the capsid, E2, and E1 envelope glycoproteins (40).The VEEV antigenic complex of alphaviruses is comprised of six antigenic subtypes (I to VI) (5). Subtype I is comprised of five varieties: AB, C, D, E, and F. Only viruses from subtypes IAB and IC have been implicated in large outbreaks of equine and human encephalitis that have occurred from northern South America to southern Texas (43,47). These viruses cause large outbreaks by e...

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Enzootic and Epizootic Venezuelan Equine Encephalomyelitis Virus in Horses Infected by Peripheral and Intrathecal Routes

Cited by 22 publications

References 13 publications

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

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

Vector Competence of Culex (Melanoconion) taeniopus for Equine-Virulent Subtype IE Strains of Venezuelan Equine Encephalitis Virus

Positively Charged Amino Acid Substitutions in the E2 Envelope Glycoprotein Are Associated with the Emergence of Venezuelan Equine Encephalitis Virus

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