Recovery of Venezuelan Equine Encephalomyelitis Virus in Panamá

Km, Johnson; Shelokov, Alexis; Ph, Peralta; Gj, Dammin; Na, Young

doi:10.4269/ajtmh.1968.17.432

Cited by 73 publications

(50 citation statements)

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“…Humans also develop relatively high titered viremia following epizootic virus infection [33][34][35] but are probably less important for amplification because they are less attractive and subject to far fewer mosquito bites than equines. Although human infections with enzootic VEE viruses can produce severe and sometimes fatal disease, [36][37][38] equines living near enzootic foci develop VEE-specific antibodies but apparently do not often suffer disease.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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 neuropathologic and neuroimmunologic effects of VEEV in human encephalitis cases have not been well described owing to lack of autopsy specimens. Gross pathologic analysis of 21 lethal encephalitis cases revealed cerebral edema and meningeal infiltrates comprised of neutrophils, lymphocytes, and monocytes that extend to Virchow Robbins spaces and, in some cases, CNS parenchyma [47].…”

Section: Togaviridaementioning

confidence: 99%

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

2016

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Arboviruses are arthropod-borne viruses that exhibit worldwide distribution, contributing to systemic and neurologic infections in a variety of geographical locations. Arboviruses are transmitted to vertebral hosts during blood feedings by mosquitoes, ticks, biting flies, mites, and nits. While the majority of arboviral infections do not lead to neuroinvasive forms of disease, they are among the most severe infectious risks to the health of the human central nervous system. The neurologic diseases caused by arboviruses include meningitis, encephalitis, myelitis, encephalomyelitis, neuritis, and myositis in which virus-and immune-mediated injury may lead to severe, persisting neurologic deficits or death. Here we will review the major families of emerging arboviruses that cause neurologic infections, their neuropathogenesis and host neuroimmunologic responses, and current strategies for treatment and prevention of neurologic infections they cause.

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“…Other symptoms range from mild nausea, vomiting with decreased sensorial capability, nuchal rigidity, ataxia and convulsions, to coma and paralysis. The fatality rate in humans is about 1 % (Johnson and Martin 1974;Johnson et al 1968;Nalca et al 2003;Pittman et al 1996). Currently, no vaccine for VEEV is publicly available and the experimental military vaccine has poor efficacy (Colpitts et al 2007;Russell 1999).…”

Section: Togaviridaementioning

confidence: 99%