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Arthropod-borne virus encephalitis
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Currently, West Nile virus disease dwarfs all other causes of arthropod-borne diseases in the United States. Surveillance data from 47 states and the District of Columbia in 2016 reported 2,240 cases of domestic arboviral disease of which 2,150 (96%) were WNV disease [14]. After WNV, La Crosse (35 cases), Powassan (22 cases), and Jamestown Canyon (15 cases) were the most frequently reported [14]. This reflects a dramatic change since the beginning of the twenty-first century, shortly after the introduction of WNV onto the North American continent. West Nile fever virus emerged in New York City in 1999, when 62 cases were identified by more intense surveillance. By 2001, human cases ranged up and down the Atlantic seaboard, and virus activity was found in animals in states west of the Mississippi River. However, despite the media attention focused on West Nile fever virus and the resulting public anxiety, it is neither the most lethal nor the most feared of the North American arboviruses. That distinction goes to Eastern equine encephalitis virus.
Mosquitoes
Published in Gail Miriam Moraru, Jerome Goddard, The Goddard Guide to Arthropods of Medical Importance, Seventh Edition, 2019
Gail Miriam Moraru, Jerome Goddard
Eastern Equine Encephalitis. Eastern equine encephalitis (EEE) is generally the most virulent, being severe and frequently fatal (mortality rate of 35–75%). In fact, half of EEE survivors suffer permanent neurologic sequelae and require long-term care costing millions of dollars.49 Fortunately, large and widespread outbreaks are not common; between 1961 and 1985 only 99 human cases were reported.50 There were six human cases reported in the U.S. in 2015.14 EEE occurs in late summer and early fall in the central and northcentral United States, parts of Canada, southward along the coastal margins of the eastern United States and the Gulf of Mexico, and sparsely throughout Central and South America (Figure 25.18). Horses are especially susceptible to EEE infection and may serve as sentinel animals to indicate virus activity in an area; however, widespread use of the eastern–western tetanus vaccine (Figure 25.19) may bias surveys of horse cases of EEE. Recently, human cases of EEE seem to be occurring more northeasterly into Maine and Vermont. The ecology of EEE is complex. The virus circulates in wild bird populations, and the exact mosquito vectors responsible for spread to humans are not well known. Some species likely involved include Aedes sollicitans, Coquillettidia perturbans, Culex salinarius, and Ae. vexans,51–53 although certain Anopheles species may serve as bridge vectors during epizootics.54
Headache associated with central nervous system infection
Published in Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby, Headache in Clinical Practice, 2018
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby
Eastern equine encephalitis produces focal radiographic signs on MRI. The characteristic early involvement of the basal ganglia (71%) and thalami (71%) distinguishes it from HSV. The presence of large lesions did not predict a poor outcome.81
Recent advances in the understanding of enterovirus A71 infection: a focus on neuropathogenesis
Published in Expert Review of Anti-infective Therapy, 2021
Han Kang Tee, Mohd Izwan Zainol, I-Ching Sam, Yoke Fun Chan
Unlike other receptors of EV-A71, HS has been previously reported to modulate neurotropism and neurovirulence in many viruses (Table 1). Overall, the mechanism of rapid virus clearance of HS-binding viruses leading to lower virus virulence has been supported by experiments in other viruses such as yellow fever virus, Japanese encephalitis virus, Murray valley encephalitis virus, West Nile virus, tick-borne encephalitis virus, Venezuelan equine encephalitis virus, coxsackie B3 virus, and dengue virus. In contrast, HS-binding viruses were associated with higher mortality in mice in Sindbis virus, Semliki Forest virus and eastern equine encephalitis virus (EEEV). Strong HS-binding EEEV antagonizes immune responses by inducing lower cytokines production, enabling higher virus replication leading to neurovirulence [131]. Interesti-ngly, EEEV with a strong HS-binding phenotype also showed higher neurovirulence in a mouse model when inoculated directly into the CNS but not by intraperitoneal injection suggesting an additional immune barrier exists during systemic infection. We have also provided a hypothesized model of EV-A71 heparin-dependent pathogenesis in humans whereby non-HS strains are associated with neurovirulence [66].
Surveillance for Zika in Mexico: naturally infected mosquitoes in urban and semi-urban areas
Published in Pathogens and Global Health, 2019
Fabián Correa-Morales, Cassandra González-Acosta, David Mejía-Zúñiga, Herón Huerta, Crescencio Pérez-Rentería, Mauricio Vazquez-Pichardo, Aldo I. Ortega-Morales, Luis M. Hernández-Triana, Víctor M. Salazar-Bueyes, Miguel Moreno-García
Female Ae. epactius have an aggressive feeding behavior, preferring to feed on mammals including humans [26]. Aedes epactius has been reported as a vector of Jamestown Canyon virus [27] and can transmit St. Louis encephalitis virus transovarially to their progeny [28]. However, Ae. epactius has never been incriminated as a vector of ZIKV, e.g., [10]. This species is a very common species in the Midwestern United States, and northern and central Mexico [15,19], including urban and suburban areas at low, mid and high elevations [29]. In urban and semi-urban areas, larvae of this species can be found in cemeteries, permanent and temporary ponds and water channels with a high content of organic matter [25]. Culex erraticus is a tropical species that occurs from South and Meso America, including southeastern Mexico, to the eastern USA, where this species reaches its northernmost distributional point [15,30]. It feeds primarily on avian hosts, however, it can also bite mammals, reptiles and amphibians [31,32]. It has been proposed that this species may have a role in Eastern Equine Encephalitis (EEE) transmission, St. Louis encephalitis (SLEV) and West Nile virus (WNV) [32]. In urban and semi-urban areas, larvae can be found in rain collectors, ponds and shipping canals [25].
Poxvirus-based vector systems and the potential for multi-valent and multi-pathogen vaccines
Published in Expert Review of Vaccines, 2018
Natalie A. Prow, Rocio Jimenez Martinez, John D. Hayball, Paul M. Howley, Andreas Suhrbier
An alternative to mixing a series of immunogens/antigens or vectors encoding single immunogens (Table 4) is the generation of single vector construct, multi-immunogen vaccines. So far the number of licensed and registered recombinant (or genetically modified) virally vectored vaccines for human use is rather low, with Dengvaxia® being the first and only current example [70]. A number of vaccine vector systems are potentially suitable for multi-valent and/or multi-pathogen vaccines [14,15,71], e.g. bacterial platforms [72], vesicular stomatitis virus (VSV) [73], varicella [74] and adenovirus [75]. However, poxvirus systems have the relatively unique capacity for large recombinant inserts [22] and have thus been widely used for development of multi-valent vaccines (Tables 1, 2, and 3). A large number of rMVA vaccines are in advanced clinical trials and many are multi-valent vaccines encoding multiple immunogens, with one rMVA multi-pathogen vaccine also in phase 1 human clinical trials (Table 2, MVA-BN-Filo). A mixed multi-pathogen rMVA vaccine targeting western equine encephalitis virus (WEEV), eastern equine encephalitis virus (EEEV) and Venezuelan equine encephalitis virus (VEEV) (Table 4) is also soon to enter clinical trials. A single-construct SCV-ZIKA/CHIK vaccine targeting ZIKV and CHIKV (viral pathogens from different viral families) is described above (and in Table 3, Figures 1 and 2).