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Chapter 3 : Recurrent Emergence of Venezuelan Equine Encephalomyelitis

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Recurrent Emergence of Venezuelan Equine Encephalomyelitis, Page 1 of 2

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Abstract:

Venezuelan equine encephalomyelitis (VEE) viruses are positive-strand, unsegmented RNA viruses in the genus Alphavirus of the family . The first phylogenetic analyses of the VEE complex, based on partial nsP4, El, and 3' untranslated sequences, indicated that IAB, IC, and ID viruses are closely related and have a recent common ancestor. This work also suggested that epidemic/epizootic VEE viruses evolved from ID progenitors on more than one occasion. Several hypotheses for VEE emergence were proposed, including (i) maintenance of IAB and/or IC viruses in continuous, cryptic transmission cycles; (ii) maintenance of IAB and/or IC viruses in latent equine or other animal infections; (iii) reemergence of epizootic viruses following administration of incompletely inactivated vaccine preparations; (iv) maintenance of IAB and/or IC viruses as minority subpopulations within enzootic virus populations; and (v) periodic emergence of epizootic viruses via mutations of enzootic strains. Phylogenetic studies of the two recent, northern South American VEE outbreaks have further supported the hypothesis of evolution and emergence of epidemic/epizootic IAB/IC viruses from enzootic ID-like progenitors. Current phylogenetic trees, obtained from reverse transcription-polymerase chain reaction products of 857 nucleotides derived from the E3 and E2 genes, identify three distinct monophyletic groups or lineages of epizootic/ epidemic VEE viruses. The most important gaps remaining in one's understanding of epidemic/epizootic VEE emergence concern the viral determinants of virulence and the pathogenesis changes that lead to high-viremia-facilitated transmission among equines and other large mammals.

Citation: Weaver S. 1998. Recurrent Emergence of Venezuelan Equine Encephalomyelitis, p 27-42. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch3
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Figures

Image of Figure 1.
Figure 1.

Map showing the locations of major VEE outbreaks.

Citation: Weaver S. 1998. Recurrent Emergence of Venezuelan Equine Encephalomyelitis, p 27-42. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch3
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Image of Figure 3.
Figure 3.

Cartoon depicting the enzootic and epidemic/epizootic transmission cycles of VEE viruses. Links between the cycles show hypothetical mechanisms of VEE emergence.

Citation: Weaver S. 1998. Recurrent Emergence of Venezuelan Equine Encephalomyelitis, p 27-42. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch3
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Image of Figure 2.
Figure 2.

Phylogenetic tree, derived by maximum parsimony ( ), showing relationships among epidemic/epizootic and enzootic; isolates of VEE viruses. The tree was generated from an E3-E2 sequence region of 817 nucleotides described previously ( ) and was rooted by using homologous sequences of other VEE subtypes. Strains are listed by abbreviated country or State (USA) and year of isolation, followed by the strain designation. Branch shading indicates hypothetical phenotype (epizootic or enzootic) of ancestral lineages, based on minimizing phenotypic change in the tree. Numbers at nodes indicate bootstrap values for groups to the right.

Citation: Weaver S. 1998. Recurrent Emergence of Venezuelan Equine Encephalomyelitis, p 27-42. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch3
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References

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Tables

Generic image for table
Table 1.

VEE antigenic complex viruses

Citation: Weaver S. 1998. Recurrent Emergence of Venezuelan Equine Encephalomyelitis, p 27-42. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch3

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