Electron microscopic observations onAedes albopictus cells infected with dengue viruses

Ko, K. K.; Igarashi, Akira; Fukai, K

doi:10.1007/bf01314902

Cited by 28 publications

(30 citation statements)

References 29 publications

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“…In medulloblasts and glioblasts, we observed similar structural abnormalities formed by membrane modifications such as the formation of SMS, ER proliferation, accumulation and convolution of membranes, which are in accordance with typical cell abnormalities described for other flavivirus infections (Matsumura et al, 1971;Ko et al, 1979;Leary & Blair, 1980;Ho et al, 1987;Ng & Hong, 1989;Chu & Westaway, 1992;Ng et al, 1994b). SMS is a typical flavivirus-induced structure associated with RER (Hase, 1993; Wang et al, 1997) that is probably formed through budding from the RER.…”

Section: Discussionsupporting

confidence: 70%

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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Section: Discussionsupporting

confidence: 70%

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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“…A common feature of flavivirus infections in cells is the proliferation of both smooth and rough endoplasmic reticula [10,13,22]. Electron microscopic studies have shown consistently the presence of mature virus particles within the lumen of the endoplasmic reticulum [7,12,14,19].…”

Section: Discussionmentioning

confidence: 98%

Flavivirus West Nile (Sarafend) egress at the plasma membrane

Howe

Sreenivasan

et al. 1994

Archives of Virology

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West Nile (Sarafend) virus was distinctly observed to bud from the plasma membrane rather than mature intracellularly. This has been observed with transmission electron microscopy. Using conventional scanning electron microscopy, budding at the plasma membrane especially at the filopodia was clearly illustrated. Immunogold labelling against the virus envelope protein was also performed to confirm this mode of exit. The gold particles were observed to be located at the sites where virus budding was seen under the field emission scanning electron microscope.

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“…Replication in both insect and mammalian cells is accompanied by the expansion of intracellular membranes (Clyde et al, 2006;Ko et al, 1979;Miller & Krijnse-Locker, 2008;Salonen et al, 2005) but a causal link between membrane amplification and virus translation and replication remains to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

A role for autophagolysosomes in dengue virus 3 production in HepG2 cells

Khakpoor

Panyasrivanit

Wikan

et al. 2009

Journal of General Virology

107

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We have recently proposed that amphisomes act as a site for translation and replication of dengue virus (DENV)-2 and that DENV-2 entry and replication are linked through an ongoing association with membranes of an endosomal-autophagosomal lineage. In this report, we present the results of an investigation into the interaction between DENV-3 and the autophagy machinery. Critically, treatment with the lysosomal fusion inhibitor L-asparagine differentiated the interaction of DENV-3 from that of DENV-2. Inhibition of fusion of autophagosomes and amphisomes with lysosomes resulted in decreased DENV-3 production, implying a role for the autophagolysosome in the DENV-3 life cycle. Evidence based upon the co-localization of LC3 and cathepsin D with double stranded RNA and NS1 protein, as assessed by confocal microscopy, support a model in which DENV-3 interacts with both amphisomes and autophagolysosomes. These results demonstrate that the interactions between DENV and the host cell autophagy machinery are complex and may be determined in part by virus-encoded factors.

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Electron microscopic observations onAedes albopictus cells infected with dengue viruses

Cited by 28 publications

References 29 publications

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

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

Flavivirus West Nile (Sarafend) egress at the plasma membrane

A role for autophagolysosomes in dengue virus 3 production in HepG2 cells

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