Development of morphological changes in experimental tick-borne meningoencephalitis induced in white mice by different virus doses

Vince, Valérie; Grcević, N

doi:10.1016/0022-510x(69)90064-1

Cited by 15 publications

(15 citation statements)

References 5 publications

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“…Inflammatory changes may occur alone, or they may be accompanied by acute swelling, degeneration, and necrosis of neurons and neuronophagia. Endothelial-cell proliferation and necrosis, perineural and perivascular edema, spongy degeneration, and focal hemorrhages are evident in some models, e.g., mice infected with TBE virus (Vince and Grcevic, 1969).…”

Section: Pathological Changes In the Central Nervous Systemmentioning

confidence: 99%

Pathobiology of the Flaviviruses

Monath

1986

The Togaviridae and Flaviviridae

105

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Section: Pathological Changes In the Central Nervous Systemmentioning

confidence: 99%

Pathobiology of the Flaviviruses

Monath

1986

The Togaviridae and Flaviviridae

105

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“…The laboratory mouse model is commonly employed to study the CNS pathology of TBEV in vivo because mice develop neurological symptoms and relatively comparable neurological dysfunction similar to that observed in humans (Chiba et al, 1999a;Pogodina and Savinov, 1964;Sokol, Libikova, and Zemla, 1959;Vince and Grcevic, 1969). However, in the mouse model of encephalitic flavivirus infection, dose-independent mortality has been an unresolved problem since the 1940's (King et al, 2007;Lennette, 1944).…”

Section: Discussionmentioning

confidence: 99%

The Development of Encephalitis Following Tick-Borne Encephalitis Virus Infection in a Mouse Model

Hayasaka¹

2011

Flavivirus Encephalitis

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“…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 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%

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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Development of morphological changes in experimental tick-borne meningoencephalitis induced in white mice by different virus doses

Cited by 15 publications

References 5 publications

Pathobiology of the Flaviviruses

Pathobiology of the Flaviviruses

The Development of Encephalitis Following Tick-Borne Encephalitis Virus Infection in a Mouse Model

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

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