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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.
Viruses
Published in Loretta A. Cormier, Pauline E. Jolly, The Primate Zoonoses, 2017
Loretta A. Cormier, Pauline E. Jolly
Alphaviruses outside of the Semliki Forest complex that have been detected in both humans and wild primates are eastern equine encephalitis virus (EEEV) and Sindbis virus. EEEV is maintained in an avian/mosquito transmission cycle in North America, South America, and the Caribbean (Markoff 2015). Culiseta species mosquitoes are most important in avian transmission, with Coquillettidia and Aedes species mosquitoes being important bridge vectors to humans, horses, and other mammals (Go et al. 2014). In Bolivia, seropositivity has been identified in Ateles species monkeys in the wild. Wild monkey, like humans and other mammals, appear to be incidentally infected. Sindbis virus belongs to the western equine encephalitis complex and, like EEEV, is maintained in an avian/mosquito transmission cycle (Markoff 2015). Culex, Culiseta, and Aedes mosquito species have been identified as important vectors (Adouchief et al. 2016). Sindbis virus occurs in Eurasia, Oceania, and South Africa (Adouchief et al. 2016). Symptoms are similar to those of the Semliki Forest complex with fever, arthralgia, and rash (Markoff 2015). Among wild primates, seropositivity has been identified in orangutans in Borneo.
Alphavirus Neurovirulence
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Katherine Taylor, Slobodan Paessler
Due to their parasitic, obligate, intracellular nature, evolution favors viruses with the ability to evade the barriers and impediments the host organism utilizes to limit their ability to replicate or cause cellular dysfunction. Avoidance of host defense mechanisms and successful replication often leads to virulence, the ability to cause fatal disease. Neurovirulent viruses alter the highly sensitive nature and critical functioning of the central nervous system (CNS) leading to fatal encephalitis or, in the event of recovery, severe neurological sequelae. With 20 viruses known to cause human encephalitis, arboviruses (arthropod-borne viruses) represent a significant public health threat as emerging infectious diseases both in the United States and worldwide. The focus of this review, arboviruses in the Alphavirus genus in the family Togaviridae, contains three viruses capable of causing human encephalitis: Venezuelan equine encephalitis virus (VEEV), eastern equine encephalitis virus (EEEV), and western equine encephalitis virus (WEEV). No specific therapy or vaccine is currently available against these viruses.
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].
Antiviral therapeutics for chikungunya virus
Published in Expert Opinion on Therapeutic Patents, 2020
Live attenuated and inactivated strains as well as DNA-based vaccine candidates have been patented. Recent advances to increase the immunogenicity of vaccine candidates include the use of CHIKV mRNA to prevent CHIKV infection as evident by promising phase I clinical trials [95]. Frolov et al. patented the chimeric CHIKV comprising structural protein of CHIKV and the non-structural protein of VEV or an Eastern equine encephalitis virus (EEV). This chimeric vaccine candidate effectively inhibited the CHIKV infection and provided wide coverage as compared to the single epitope. Similarly, other multivalent vaccines could be developed to target the viruses that can coexist. Moreover, the patent application by ModernaTX, Inc. claims the lipid nanoparticle encapsulating the RNA encoding envelop glycoproteins of CHIKV. These nanoparticles elicited strong immune response and can be used as potential therapeutics [60,105].
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).