Western Equine and St. Louis Encephalitis

Finley, Knox H.; Longshore, W. A.; Palmer, Richard J.; Cook, Robert E.; Riggs, Naomi

doi:10.1212/wnl.5.4.233

Cited by 37 publications

(12 citation statements)

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“…Indeed, in cases of viral encephalitis such as from human herpesvirus 6 (HHV6), there was significant damage to the medial temporal lobe including the amygdala (Provenzale et al 2008). Neurological sequelae in patients surviving alphavirus encephalomyelitis have been reported to include hyperactivity, emotional disinhibition, and temperament disturbances (Bruyn and Lennette 1953; Finley et al 1955; Earnest et al 1971; Villari et al 1995), and symptoms similar to attention-deficit/hyperactivity disorder have been described in patients affected by encephalitis caused by other types of viruses, such as HIV (Nozyce 2006; Millichap 2008). …”

Section: Discussionmentioning

confidence: 99%

“…The New World alphaviruses, which include eastern equine encephalitis virus (EEEV), western equine encephalitis virus (WEEV), and Venezuelan equine encephalitis virus (VEEV), cause encephalomyelitis in humans and horses with varying rates of mortality (Steele et al 2007; Griffin 2013). Many patients that recover from the acute clinical disease, especially infants and children, are left with life-long debilitating neurological defects, such as cognitive deficits, impaired motor control, and emotional and behavioral disturbances (Bruyn and Lennette 1953; Finley et al 1955; Earnest et al 1971; Villari et al 1995). Currently, no treatments beyond symptomatic care are available, and no licensed human vaccines exist (Griffin 2010).…”

Section: Introductionmentioning

confidence: 99%

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Neurological sequelae induced by alphavirus infection of the CNS are attenuated by treatment with the glutamine antagonist 6-diazo-5-oxo-l-norleucine

et al. 2015

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Recovery from encephalomyelitis induced by infection with mosquito-borne alphaviruses is associated with a high risk of lifelong debilitating neurological deficits. Infection of mice with the prototypic alphavirus, Sindbis virus, provides an animal model with which to study disease mechanisms and examine potential therapeutics. Infectious virus is cleared from the brain within a week after infection, but viral RNA is cleared slowly and persists for the life of the animal. However, no studies have examined the effect of infection on neurocognitive function over time. In the present study, we examined neurocognitive function at different phases of infection in five-week-old C57BL/6 mice intranasally inoculated with Sindbis virus. At the peak of active virus infection, mice demonstrated hyperactivity, decreased anxiety, and marked hippocampal-dependent memory deficits, the latter of which persisted beyond clearance of infectious virus and resolution of clinical signs of disease. Previous studies indicate that neuronal damage during alphavirus encephalomyelitis is primarily due to inflammatory cell infiltration and glutamate excitotoxicity rather than directly by virus infection. Therefore, mice were treated with 6-diazo-5-oxo-l-norleucine (DON), a glutamine antagonist that can suppress both the immune response and excitotoxicity. Treatment with DON decreased inflammatory cell infiltration and cell death in the hippocampus and partially prevented development of clinical signs and neurocognitive impairment despite the presence of infectious virus and high viral RNA levels. This study presents the first report of neurocognitive sequelae in mice with alphavirus encephalomyelitis and provides a model system for further elucidation of the pathogenesis of virus infection and assessment of potential therapies.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neurological sequelae induced by alphavirus infection of the CNS are attenuated by treatment with the glutamine antagonist 6-diazo-5-oxo-l-norleucine

et al. 2015

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“…Clinical symptoms are most common in the very young and those older than 50 years (Longshore et al, 1956). Severe disease, seizures, fatal encephalitis, and significant sequelae are more likely to occur in infants and young children (Kokernot et al, 1953;Finley et al, 1955;Earnst et al, 1971). In areas of endemic disease, seroprevalence in humans is fairly common.…”

Section: Western Equine Encephalitis Virusmentioning

confidence: 99%

Vaccines and animal models for arboviral encephalitides

2003

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“…tarsalis mosquitoes 12,13 and caused neuroinvasive illness. [14][15][16] In recent decades, encephalitis cases in humans and horses caused by WEEV infections have almost disappeared from western North America because of increased equine vaccination, 17 improved irrigation practices that reduce standing water, 18 expanded vector control and surveillance, and human behavioral changes that have reduced exposure to mosquitoes. 19 However, enzootic WEEV activity is still detected sporadically in many areas of California, 20,21 with activity during some years involving extensive areas.…”

Section: Introductionmentioning

confidence: 99%

Temporal Connections between Culex tarsalis Abundance and Transmission of Western Equine Encephalomyelitis Virus in California

Barker¹,

Johnson²,

Eldridge³

et al. 2010

The American Society of Tropical Medicine and Hygiene

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Definition of targets for vector control requires an understanding of the relationship between vector abundance and the intensity of arbovirus transmission. Using an extensive surveillance dataset with observations from sentinel chicken flocks and mosquito traps paired in time and space, hierarchical autoregressive logistic regression models were developed to predict the probability of seroconversion in chickens for western equine encephalomyelitis virus (WEEV) based on the relative abundance of the principal vector, Culex tarsalis. After adjustments for confounders, the abundance of Cx. tarsalis 29–42 d before the date of chicken sampling was credibly associated with the risk of WEEV transmission in both the Central and Coachella Valleys, and a doubling of relative Cx. tarsalis abundance was associated with a 58% increase in the odds of seroconversion. The critical time windows identified in our study highlight the need for surveillance of vector populations and forecasting models to guide proactive vector control measures before the detection of transmission to sentinel chickens.

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Western Equine and St. Louis Encephalitis

Cited by 37 publications

References 0 publications

Neurological sequelae induced by alphavirus infection of the CNS are attenuated by treatment with the glutamine antagonist 6-diazo-5-oxo-l-norleucine

Neurological sequelae induced by alphavirus infection of the CNS are attenuated by treatment with the glutamine antagonist 6-diazo-5-oxo-l-norleucine

Vaccines and animal models for arboviral encephalitides

Temporal Connections between Culex tarsalis Abundance and Transmission of Western Equine Encephalomyelitis Virus in California

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