Venezuelan Equine Encephalitis in Panama: Fatal Endemic Disease and Genetic Diversity of Etiologic Viral Strains

Quiroz, Evelia; Aguilar, Patricia V.; Cisneros, Julio Zúñiga; Tesh, Robert B.; Weaver, Scott C.

doi:10.1371/journal.pntd.0000472

Cited by 54 publications

(77 citation statements)

References 34 publications

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“…Both fatal cases described in this report were clinically similar to previously reported enzootic and epidemic VEE cases ( 1 , 6 , 8 , 9 , 11 , 14 ). Initially, both patients had fever, body aches, vomiting, and diarrhea (Table 1) ( 1 , 6 , 8 , 9 , 11 ), which are also caused by other tropical diseases like dengue.…”

Section: Discussionsupporting

confidence: 89%

Venezuelan Equine Encephalitis and 2 Human Deaths, Peru

Vilcarromero¹,

Aguilar²,

Halsey³

et al. 2010

Emerg. Infect. Dis.

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Section: Discussionsupporting

confidence: 89%

Venezuelan Equine Encephalitis and 2 Human Deaths, Peru

Vilcarromero¹,

Aguilar²,

Halsey³

et al. 2010

Emerg. Infect. Dis.

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“…Most cases of human and equine disease have been associated with epizootic VEEV strains (subtypes IAB and IC) that undergo efficient amplification within horses, but recent studies indicate that endemic transmission of equine avirulent strains (subtype ID) is responsible for many unreported cases in humans that live near habitats where enzootic transmission occurs (2,46,57). When infected via the mosquito vector, patients may present with malaise, fever, and headache (57).…”

mentioning

confidence: 99%

Venezuelan Equine Encephalitis Virus Disrupts STAT1 Signaling by Distinct Mechanisms Independent of Host Shutoff

Simmons

White

Morrison

et al. 2009

J Virol

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Venezuelan equine encephalitis virus (VEEV) is an important human and veterinary pathogen causing sporadic epizootic outbreaks of potentially fatal encephalitis. The type I interferon (IFN) system plays a central role in controlling VEEV and other alphavirus infections, and IFN evasion is likely an important determinant of whether these viruses disseminate and cause disease within their hosts. Alphaviruses are thought to limit the induction of type I IFNs and IFN-stimulated genes by shutting off host cell macromolecular synthesis, which in the case of VEEV is partially mediated by the viral capsid protein. However, more specific strategies by which alphaviruses inhibit type I IFN signaling have not been characterized. Analyses of cells infected with VEEV and VEEV replicon particles (VRP) demonstrate that viral infection rapidly disrupts tyrosine phosphorylation and nuclear translocation of the transcription factor STAT1 in response to both IFN-␤ and IFN-␥. This effect was independent of host shutoff and expression of viral capsid, suggesting that VEEV uses novel mechanisms to interfere with type I and type II IFN signaling. Furthermore, at times when STAT1 activation was efficiently inhibited, VRP infection did not limit tyrosine phosphorylation of Jak1, Tyk2, or STAT2 after IFN-␤ treatment but did inhibit Jak1 and Jak2 activation in response to IFN-␥, suggesting that VEEV interferes with STAT1 activation by the type I and II receptor complexes through distinct mechanisms. Identification of the viral requirements for this novel STAT1 inhibition will further our understanding of alphavirus molecular pathogenesis and may provide insights into effective alphavirus-based vaccine design.Venezuelan equine encephalitis virus (VEEV) is a mosquitoborne alphavirus in the family Togaviridae that is responsible for sporadic epidemics of encephalitis in equines and humans. Most cases of human and equine disease have been associated with epizootic VEEV strains (subtypes IAB and IC) that undergo efficient amplification within horses, but recent studies indicate that endemic transmission of equine avirulent strains (subtype ID) is responsible for many unreported cases in humans that live near habitats where enzootic transmission occurs (2,46,57). When infected via the mosquito vector, patients may present with malaise, fever, and headache (57). While fatalities are rare (Ͻ1%), patients that recover from encephalitis may suffer from permanent neurological sequelae (30).The type I interferons (IFNs) ␣ and ␤ represent a crucial innate defense system against most viral pathogens, including alphaviruses. These cytokines act in autocrine and paracrine pathways to induce the expression of numerous IFN-stimulated genes (ISGs), such as 2Ј,5Ј-OAS, PKR, and Mx family members that are important for the control of viral infection (reviewed in reference 20). The signaling events that follow IFN stimulation have been well described (reviewed in references 31 and 42). In brief, when the type I IFNs bind the IFN-␣/␤ receptor subunits IFNAR1 and...

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“…Neurological and/or fatal disease after VEEV subtype ID infection has been documented in Bolivia, Colombia, Panama and Peru [68,75,85]. Hemorrhagic manifestations have also been described in patients infected with subtype ID viruses in Panama and Peru [68,84].…”

Section: Vee Complexmentioning

confidence: 99%

“…Furthermore, Aedes albopictus , which is present in both tropical and temperate regions, is also an efficient laboratory vector [109]. Thus, human viremia levels after infection with both endemic [75] and epizootic VEEV strains [22,110], combined with urban vector susceptibility, could potentially lead to a stable, endemic, urban VEEV cycle that could have devastating public health implications throughout Latin America.…”

Section: Future Perspectivementioning

confidence: 99%

Addressing theFertility needs of HIV-Seropositive Males

et al. 2011

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Venezuelan equine encephalitis (VEE) is an emerging infectious disease in Latin America. Outbreaks have been recorded for decades in countries with enzootic circulation, and the recent implementation of surveillance systems has allowed the detection of additional human cases in countries and areas with previously unknown VEE activity. Clinically, VEE is indistinguishable from dengue and other arboviral diseases and confirmatory diagnosis requires the use of specialized laboratory tests that are difficult to afford in resource-limited regions. Thus, the disease burden of endemic VEE in developing countries remains largely unknown, but recent surveillance suggests that it may represent up to 10% of the dengue burden in neotropical cities, or tens-of-thousands of cases per year throughout Latin America. The potential emergence of epizootic viruses from enzootic progenitors further highlights the need to strengthen surveillance activities, identify mosquito vectors and reservoirs and develop effective strategies to control the disease. In this article, we provide an overview of the current status of endemic VEE that results from spillover of the enzootic cycles, and we discuss public health measures for disease control as well as future avenues for VEE research.

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Venezuelan Equine Encephalitis in Panama: Fatal Endemic Disease and Genetic Diversity of Etiologic Viral Strains

Cited by 54 publications

References 34 publications

Venezuelan Equine Encephalitis and 2 Human Deaths, Peru

Venezuelan Equine Encephalitis and 2 Human Deaths, Peru

Venezuelan Equine Encephalitis Virus Disrupts STAT1 Signaling by Distinct Mechanisms Independent of Host Shutoff

Addressing theFertility needs of HIV-Seropositive Males

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