Pathogenicity of tick-borne encephalitis virus isolated in Hokkaido, Japan in mouse model

Chiba, Nobuyuki; Iwasaki, Takuya; Mizutani, Tetsuya; Kariwa, Hiroaki; Kurata, Takeshi; Takashima, Ikuo

doi:10.1016/s0264-410x(98)00262-x

Cited by 48 publications

(42 citation statements)

References 20 publications

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“…However, our previous studies in a mouse model found that peripheral infection with the Oshima strain of TBEV caused a dose-independent mortality [2,9]. Furthermore, we showed that following peripheral infection mice died either early or late and that mortality resulted from a combination of CNS pathology, systemic stress and inflammatory responses [9].…”

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confidence: 58%

“…On the other hand, our previous studies showed that peripheral infection with the Oshima strain of TBEV caused dose-independent mortality [2,9]. Furthermore, depending on the dose of virus administered, a proportion of the mice died either early or late, or recovered following the onset of CNS disease [9].…”

Section: Discussionmentioning

confidence: 96%

“…Direct viral infection of neurons is considered to be the major cause of neurological disease because viral infections cause apoptosis or degeneration of neurons in vivo and in vitro [3,11,18,21]. In addition, recent studies have demonstrated that immunopathological effects also contribute to the severity of CNS pathology [19,27].The laboratory mouse model is the system most commonly employed to study the CNS pathology of TBEV in vivo [2,17,22,26]. The CNS pathology of TBEV consists of the two distinct features of neuroinvasiveness and neurovirulence, and death has been used as an index of pathogenesis [13,15].…”

mentioning

confidence: 99%

“…The CNS pathology of TBEV consists of the two distinct features of neuroinvasiveness and neurovirulence, and death has been used as an index of pathogenesis [13,15]. Thus, mortality following peripheral infection is considered to represent neuroinvasiveness, whereas mortality following direct intracerebral infection represents neurovirulence [13].However, our previous studies in a mouse model found that peripheral infection with the Oshima strain of TBEV caused a dose-independent mortality [2,9]. Furthermore, we showed that following peripheral infection mice died either early or late and that mortality resulted from a combination of CNS pathology, systemic stress and inflammatory responses [9].…”

mentioning

confidence: 99%

“…The laboratory mouse model is the system most commonly employed to study the CNS pathology of TBEV in vivo [2,17,22,26]. The CNS pathology of TBEV consists of the two distinct features of neuroinvasiveness and neurovirulence, and death has been used as an index of pathogenesis [13,15].…”

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confidence: 99%

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Early Mortality Following Intracerebral Infection with the Oshima Strain of Tick-Borne Encephalitis Virus in a Mouse Model

et al. 2010

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ABSTRACT. Tick-borne encephalitis virus (TBEV) is a zoonotic agent that causes acute central nervous system (CNS) disease in humans. In this study, we examined the pathogenic process following intracerebral infection with the Oshima strain of TBEV in a mouse model. Intracerebral infection resulted in dose-dependent mortality, and all mice died following challenge with 10 2 PFU or more of the virus within 10 days. Acutely necrotic neurons and widespread inflammation were observed throughout the CNS. We therefore conclude that mortality following intracerebral infection results from a direct CNS pathology.KEY WORDS: central nervous system, mouse, pathogenesis, Tick-borne disease, virus infection.J. Vet. Med. Sci. 72(4): 391-396, 2010 Tick-borne encephalitis virus (TBEV), belonging to the genus Flavivirus in the family Flaviviridae, is a zoonotic agent of acute central nervous system (CNS) disease in humans [4,12]. TBEV is transmitted by Ixodes tick species and rodents in nature and infects humans through the bite of an infected tick [12]. TBEV is geographically and genetically divided into three subtypes comprising the European, Siberian and far eastern subtypes [5,8]. Our previous data showed that TBEV is also distributed throughout southern parts of Hokkaido, Japan [23][24][25].In human cases, the neurological symptoms include fever, headache, meningitis, meningoencephalitis and meningoencephalomyelitis, the latter being observed in the most severe cases [4]. When death follows, it is usually within 5 to 7 days of the onset of neurological signs. The pathological findings in the brain in human cases are nonspecific, and lesions containing TBEV antigens are located in the brain stem, cerebrum, cerebellar cortex, pons, cerebellum, thalamus and motor neurons [4,6,7]. Thus, the clinical features are not unique to TBE, and laboratory diagnosis is required to distinguish it from other neurological disorders [1,10,14].CNS pathology following TBEV infection is the consequence of viral infection of the corresponding cells and the resulting inflammatory responses in the CNS. Direct viral infection of neurons is considered to be the major cause of neurological disease because viral infections cause apoptosis or degeneration of neurons in vivo and in vitro [3,11,18,21]. In addition, recent studies have demonstrated that immunopathological effects also contribute to the severity of CNS pathology [19,27].The laboratory mouse model is the system most commonly employed to study the CNS pathology of TBEV in vivo [2,17,22,26]. The CNS pathology of TBEV consists of the two distinct features of neuroinvasiveness and neurovirulence, and death has been used as an index of pathogenesis [13,15]. Thus, mortality following peripheral infection is considered to represent neuroinvasiveness, whereas mortality following direct intracerebral infection represents neurovirulence [13].However, our previous studies in a mouse model found that peripheral infection with the Oshima strain of TBEV caused a dose-independent mortality [2,9]. Further...

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confidence: 58%

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confidence: 96%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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Early Mortality Following Intracerebral Infection with the Oshima Strain of Tick-Borne Encephalitis Virus in a Mouse Model

et al. 2010

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Characterisation of human tick‐borne encephalitis virus from Sweden

Haglund

Vene

Forsgren

et al. 2003

Journal of Medical Virology

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Viruses of the tick-borne encephalitis (TBE) antigenic complex, within the family Flaviviridae, cause a variety of diseases including uncomplicated febrile illness, meningo-encephalitis and haemorrhagic fever. Different wildlife species act as reservoir hosts with ixodid tick species as vectors. TBE virus (TBEV) causes 40-130 cases confirmed serologically in Sweden each year. Characteristics of TBEV strains circulating in Sweden have not been investigated previously and no viral sequence data has been reported. In the present study, virus strains were isolated from serum of patients with clinical symptoms consistent with acute TBEV infection. Serologic characterisation, using a panel of E-specific monoclonal antibodies and cross-neutralisation tests, indicated that the Swedish strains of TBEV, isolated 1958-1994, all belonged to the Western TBEV subtype, which includes the Austrian vaccine strain Neudoerfl. Genetic analysis of a partial E-sequence confirmed this close relationship: all Swedish TBEV strains belonged to the European lineage of the Western TBEV subtype, which includes the previously characterised strains Neudoerfl, Hypr, and Kumlinge. Further, three Swedish strains showed partial E-sequences identical to that of the Finnish Kumlinge strain, ten Swedish strains formed a well-supported separate cluster, whereas four others did not show any real clustering. No apparent correlation was observed in comparison of clinical parameters with genetic data or geographic origin of the strains.

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Clinical evaluation of highly pathogenic tick‐borne flavivirus infection in the mouse model

Tigabu

Juelich

Joseph

et al. 2009

Journal of Medical Virology

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The objective of this study was to evaluate the feasibility of using clinical parameters to demonstrate disease progression and differentiate between Omsk hemorrhagic fever virus (OHFV) and Russian spring-summer encephalitis virus (RSSEV) infection in the mouse model. Adult C57BL/6 and balb/c mice were infected with either OHFV or RSSEV by footpad inoculation and their temperature, body weight, clinical signs complete blood count, and blood chemistries were evaluated for up to 15 days post-infection (dpi). Clinical evaluation showed that OHFV infection seriously affects balb/c mice, which had shorter average survival times (ASTs) than other groups. On the contrary, RSSEV infection of C57BL/6 mice was more severe than in balb/c mice. During these studies, the development of fever was not observed and the body weight of OHFV infected balb/c and C57BL/6 mice began to decline sharply starting from day 7 and 8, respectively, which correlated with disease onset. Peak increase of globulin and neutrophils was demonstrated after 9 dpi in OHFV infected mice; however, the lymphocyte number was not affected. Viremia was undetectable in these animals with either virus infection, but virus was found in most organs tested. These results indicate marked differences in the clinical signs, pathology, and immune response of mice infected with either OHFV or RSSEV and further validate the use of this mouse model system to evaluate human disease.

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Pathogenicity of tick-borne encephalitis virus isolated in Hokkaido, Japan in mouse model

Cited by 48 publications

References 20 publications

Early Mortality Following Intracerebral Infection with the Oshima Strain of Tick-Borne Encephalitis Virus in a Mouse Model

Early Mortality Following Intracerebral Infection with the Oshima Strain of Tick-Borne Encephalitis Virus in a Mouse Model

Characterisation of human tick‐borne encephalitis virus from Sweden

Clinical evaluation of highly pathogenic tick‐borne flavivirus infection in the mouse model

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