Comparison of replication rates and pathogenicities between the SA 14 parent and SA 14-14-2 vaccine strains of Japanese encephalitis virus in mouse brain neurons

Hase, Tatsuo; Dubois, Doria R.; Summers, Peter L.; Downs, M; Ussery, Michael A.

doi:10.1007/bf01319002

Cited by 20 publications

(6 citation statements)

References 21 publications

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“…The site of replication was sur- rounded by numerous mitochondria. The results are in accordance with observations of the infection of TBEV in neuronal cell cultures [13] as well as other flavivirus infections (Japanese encephalitis virus infection of cultured neurons [15] , but also the infection of mouse brain neurons and BHK-21 cells with Japanese encephalitis virus [16][17][18] and other viral infections [14] ).…”

supporting

confidence: 80%

Tick-Borne Encephalitis Virus Infection of Cultured Mouse Macrophages

Ahantarig

Růžek²,

Vancová³

et al. 2009

Intervirology

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The interactions of tick-borne encephalitis virus (TBEV) with mouse macrophages were studied at the electron microscopic level. The cultured mouse macrophages were sensitive to infection with TBEV strain Hypr (a highly neuroinvasive and neurovirulent strain for laboratory mice) and produced relatively high virus titers. However, these macrophage cells remained morphologically inactivated. Viral particles were located mainly in the ER but were also present in other exocytic compartments. No virus production was observed in cells infected with the attenuated, non-neuroinvasive TBEV strain 263. In this case, the infection led to a clear morphological activation of the macrophages. In conclusion, the virus replication process in mouse macrophage cells might be different from that in other mammalian cell lines since the smooth membrane structures, which are thought to be the sites for flavivirus replication, were not observed. Moreover, different TBEV strains exhibited a different interaction with the host macrophages. The inability of strain 263 to replicate in mouse macrophages as the first site of significant viral replication in vivo could be associated with the inability of this strain to establish a serious infection in mice.

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supporting

confidence: 80%

Tick-Borne Encephalitis Virus Infection of Cultured Mouse Macrophages

Ahantarig

Růžek²,

Vancová³

et al. 2009

Intervirology

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“…The induction of membrane rearrangement has also been described in other flavivirus infections. Similar dilation of RER with the presence of numerous virions and SMS-like particles was described in cultured mouse neurons and BHK-21 cells infected by JEV (Hase, 1993;Hase et al, 1993;Takegami et al, 1995; Wang et al 1997). SMS and smooth convoluted membranes have been described as the site of virus replication in Kujin virus-infected Vero cells (Westaway et al, 1997;.…”

mentioning

confidence: 59%

Morphological changes in human neural cells following tick-borne encephalitis virus infection

Růžek

Vancová

Tesařová

et al. 2009

Journal of General Virology

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Tick-borne encephalitis (TBE) is one of the leading and most dangerous human viral neuroinfections in Europe and north-eastern Asia. The clinical manifestations include asymptomatic infections, fevers and debilitating encephalitis that might progress into chronic disease or fatal infection. To understand TBE pathology further in host nervous systems, three human neural cell lines, neuroblastoma, medulloblastoma and glioblastoma, were infected with TBE virus (TBEV). The susceptibility and virus-mediated cytopathic effect, including ultrastructural and apoptotic changes of the cells, were examined. All the neural cell lines tested were susceptible to TBEV infection. Interestingly, the neural cells produced about 100-to 10 000-fold higher virus titres than the conventional cell lines of extraneural origin, indicating the highly susceptible nature of neural cells to TBEV infection. The infection of medulloblastoma and glioblastoma cells was associated with a number of major morphological changes, including proliferation of membranes of the rough endoplasmic reticulum and extensive rearrangement of cytoskeletal structures. The TBEV-infected cells exhibited either necrotic or apoptotic morphological features. We observed ultrastructural apoptotic signs (condensation, margination and fragmentation of chromatin) and other alterations, such as vacuolation of the cytoplasm, dilatation of the endoplasmic reticulum cisternae and shrinkage of cells, accompanied by a high density of the cytoplasm. On the other hand, infected neuroblastoma cells did not exhibit proliferation of membranous structures. The virions were present in both the endoplasmic reticulum and the cytoplasm. Cells were dying preferentially by necrotic mechanisms rather than apoptosis. The neuropathological significance of these observations is discussed. INTRODUCTIONTick-borne encephalitis virus (TBEV) is the most medically important member of the tick-borne group of the genus Flavivirus within the family Flaviviridae (Thiel et al., 2005). The virus represents a causative agent of tick-borne encephalitis (TBE), a severe infection of the central nervous system (CNS) (Gritsun et al., 2003), which is prevalent throughout wide areas in Europe and Asia.The nature of the host cell response to TBEV infection remains undefined. Characteristic, but not disease-specific neuropathologic changes in the CNS include meningitis and polioencephalomyelitis predominantly in the spinal cord, brainstem and cerrebellum associated with inflammatory cell infiltration. These pathological changes have been described in mice (Osetowska & Wró blewskaMularczyk, 1966; Rů žek et al., 2009), hamsters (Simon et al., 1966), monkeys (Simon et al., 1967 and humans (Seitelberger & Jellinger, 1966; Környey, 1978;Beer et al., 1999; Schellinger et al., 2000; Gelpi et al., 2005 Gelpi et al., , 2006. Although cytopathic effects (CPEs) have been observed primarily in virus-infected neurons, other cells can also exhibit pathological changes, presumably through bystander injury.To clarify the inter...

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“…Experimental evidence in support of this is based on the known propensity of arboviruses to infect and spread more rapidly through nervous tissue of young rodents; however, resistance to fatal infection occurs abruptly soon after the weanling stage. This resistance occurs in conjunction with neural ontogeny and is associated with restricted replication of virus in neurons as a function of their degree of differentiation, with low levels of virus being observed in mature neurons in some models (Hase et al, 1993;Ogata et al, 1991). However, this phenomenon is very dependent on the intrinsic level of viral neurovirulence, being most apparent with strains of lower virulence (Eldadah et al, 1967a;Ogata et al, 1991;Oliver et al, 1997), and is also affected by the dose and route of inoculation (Eldadah et al, 1967a;Fitzgeorge and Bradish, 1980).…”

Section: Host Factorsmentioning

confidence: 99%

“…Flaviviruses, particularly members of the JEV and TBEV serogroups, cause viral encephalitis in many vertebrate species, a deadend transmission pathway believed to reflect an evolutionarily conserved capacity of these viruses to grow in the CNS of arthropods and vertebrates (Monath, 1986). In contrast to the noncytopathic nature of infection in arthropods, a spectrum of acute and chronic CNS pathologic changes occur in vertebrates and have been documented extensively (Chu et al, 1999;Dominguez and Baruch, 1963;Hase et al, 1993;Levenbook et al, 1987;Manuelidis, 1956;Nathanson et al, 1966;Pogodina et al, 1983;Reyes et al, 1981;Vince and Grevic, 1969;Zlotnik et al, 1971Zlotnik et al, , 1976. Virus can be demonstrated within neurons throughout the brain and spinal cord, but infection of other cell types has been less well characterized.…”

Section: Neuropathologymentioning

confidence: 99%