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Viral Pathogens: A General Account
Published in Jagriti Narang, Manika Khanuja, Small Bite, Big Threat, 2020
Vinod Joshi, Bennet Angel, Annette Angel, Neelam Yadav, Jagriti Narang
This is yet another virus belonging to the family Flaviviridae. It is named so as it was first identified in Japan in 1871 and is characterized by paralysis and encephalitis-like symptoms in severe stages. Japanese encephalitis virus (JEV) is actually one of the viruses falling under the JE serogroup. This group includes viruses causing encephalitis-like West Nile virus, St. Louis encephalitic virus, and Murray Valley encephalitis virus (Gould et al., 2003). The JEV has five genotypes, namely GI to GV, each having a unique distribution pattern. The Indonesia-Malaysia region has all the five genotypes circulating, the Taiwan-Philippines region has GII and GIII circulating, the Thailand-Cambodia-Vietnam region has GI-GIII circulating, the Australia-New Guinea region has GI-II circulating, the Japan-Korea-China region has GI and GIII circulating, while India-Sri Lanka-Nepal has GIII circulating (Fig. 3.9) (Solomon et al., 2003; Yun et al., 2003).
Arthropod-borne virus encephalitis
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
In the years between 1917 and 1925, Australia experienced several outbreaks of a highly lethal encephalitis [153]. It was called Australian X disease to distinguish it from von Economo’s disease, which was raging worldwide during those years. Virus was isolated but lost in subsequent years [15]. In 1951 the disease reappeared in the Murray River and Darling River areas, and was called Murray Valley encephalitis. Virus was isolated and characterized as a group B arbovirus [153]. Since the isolate of Australian X disease had been lost, identity of the agents could not be achieved, but clinical and epidemiologic features led to the conclusion that they were in fact identical [154]. Following an outbreak in 1974, the illness was called Australian encephalitis [153]. However, Australian encephalitis also includes cases due to Kunjin virus [155], a flavivirus, related to Murray Valley encephalitis virus (MVEV), but most closely related to West Nile virus.
Murray Valley Encephalitis Virus
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Natalie A. Prow, Roy A. Hall, Mario Lobigs
Murray Valley encephalitis (MVE) is an important mosquito-borne viral disease of Australia that causes annual, sporadic cases and occasional epidemics of potentially fatal encephalitis in man. Although human cases of the disease are most commonly reported in the tropical areas of Northern Australia, ecological factors and climatic conditions occasionally result in cases appearing in more southerly areas of the country, sometimes involving large-scale outbreaks of the disease. As there are no virus-specific vaccines or treatment options currently available, this vector-borne viral disease continues to represent a major public health threat in Australia. In this chapter we discuss properties of the virus, cellular infection, clinical disease and the host immune response to infection. We also describe recent advances in diagnosis of the disease and strategies for disease prevention.
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].
Alfred Walter Campbell’s return to Australia
Published in Journal of the History of the Neurosciences, 2018
What do we make today of Campbell’s Australian research? His demolition of Bolk’s 1903–1906 version of his hypothesis of cerebellar localisation was complete. That it has never been revived in that form is, however, not due to Campbell, whose work remained unknown outside of Australia. His understanding of the neuroses and psychoses in war was ahead of its time and was still regarded of value when World War II broke. His priority in the cytoarchitectonics of the gorilla brain cannot be challenged, of course, but neither have his findings. About his work on what came to be known as Murray Valley encephalitis, Macfarlane Burnet—virologist, immunologist, and Nobel laureate—said that the work of Cleland, Bradley, and Campbell provided “the first recognition of a disease of the type we now call the insect-borne encephalitides and the first ‘isolation’ of one of the viruses responsible” (Burnet 1952, p. 1519).
Recent developments in vaccines and biological therapies against Japanese encephalitis virus
Published in Expert Opinion on Biological Therapy, 2018
Immunogenicity of cell culture-derived inactivated JEV vaccines can be improved by combination with new adjuvants, such as Advax delta inulin, a polysaccharide-based adjuvant. Immunization of mice and horses with two doses of Advax-adjuvanted JEV-inactivated vaccine was shown to induce a robust neutralizing antibody response, comparable to that elicited with live ChimeriVax-JE immunization, and cross-neutralizing antibodies against other flaviviruses belonging to the JEV serocomplex, including Murray Valley encephalitis virus and WNV [120]. The mechanism of protection of the Advax-adjuvanted vaccine was related to the induction of memory B cell response, which provided long-lived protection against JEV [121] and cross-protection against heterologous flaviviruses [122].