Morphogenesis of Flaviviruses

Hase, Tatsuo; Summers, Peter L.; Eckels, Kenneth H.; Putnak, J. Robert

doi:10.1007/978-1-4899-1675-4_9

Cited by 19 publications

(13 citation statements)

References 119 publications

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“…Generally, flavivirus-infected cells exhibit two modes of maturation, termed cis and trans (Hase et al, 1989). In trans mode maturation, virus particles are assembled in the RER and associated membraneous structures.…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 99%

“…5c, d). However, the role of the cytoskeletal network in TBEV replication still remains largely unknown and is worth investigating in the future.Generally, flavivirus-infected cells exhibit two modes of maturation, termed cis and trans (Hase et al, 1989). In trans mode maturation, virus particles are assembled in the RER and associated membraneous structures.…”

mentioning

confidence: 99%

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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“…Thus, the results of both the virus titration and morphological observation indicated that, following intracerebral inoculation into mice, the SA 14 parent strain of JE virus replicated vigorously and spread rapidly to a majority of neurons in the mouse brain, while the SA 14-14-2 strain replicated poorly and infected only a small number of neurons in scattered small foci before disappearing. Since JE virus replicates by trans-type maturation [6,9], it is believed that the viral growth in host cells occurs in the following sequence: (a) viral entry and uncoating at the cell surface, (b) viral replication at smooth endoplasmic reticulum (SER) and viral translation on RER, (c) viral assembly and maturation in the host-cell secretory channel, and (d) viral release into the extracellular space by secretory-type exocytosis. Therefore, it seems reasonable to believe that poor viral replication results from either partial impairment or complete blockage of one or more of the above processes.…”

Section: Discussionmentioning

confidence: 99%

“…After attachment to the cell surface, JE virus enters host cells by directly penetrating through the plasma membrane and uncoats [7,8,12]. JE virus genome released into the cytoplasm replicates genomic RNA and translates viral proteins on the endoplasmic reticulum membranes and discharges the viral products into the rough endoplasmic reticulum (RER) cisternae for viral assembly [9]. The progeny virions assembled in the cisternae are released extracellularly through the host-cell secretory channel via the Golgi apparatus by secretory-type exocytosis [6,10,17].…”

Section: Introductionmentioning

confidence: 99%

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

Dubois

Summers

et al. 1993

Archives of Virology

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“…4). In both cell types SLE virus undergoes trans-type maturation (Hase et al, 1989). During this process viral products are either synthesized or transported into the cisternae of the rough endoplasmic reticulum (RER) where formation of the nucleocapsid and assembly of the envelope are coordinated to produce mature virions.…”

Section: St Louis Encephalitis (Sle) Virus a Member Of The Familymentioning

confidence: 99%

St Louis encephalitis virus establishes a productive, cytopathic and persistent infection of Sf9 cells

Zhang

Klutch²,

Müller³

et al. 1993

Journal of General Virology

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The Sf9 cell line, commonly used for gene expression by recombinant baculovirus, has been productively infected by St Louis encephalitis (SLE) virus, a flavivirus. SLE viral infection produced a c.p.e, in the SO cells characterized by giant cells and the presence of 10-fold fewer cells in the infected cultures after the first week of infection compared with uninoculated control cultures. Infected Sf9 cells expressed SLE viral antigens, and intracellular virus particles were observed by electron microscopy. Titres of cell-associated SLE virus rose slightly over an 8 week period, whereas titres of cell-free virus remained stable, suggesting that SLE virus establishes a productive and persistent infection of Sf9 cells. The SLE virus produced by the Sf9 cells could be neutralized by SLE virus-immune mouse ascitic fluid, and no evidence of escape mutants was detected. Sf9 cells persistently infected with SLE virus could be superinfected with a recombinant baculovirus and expressed recombinant antigen. The successful infection of SD cells by SLE virus represents the first report of production of c.p.e, by SLE virus in insect cells under routine cell culture conditions and of the infection of Sf9 cells by a human pathogen.

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Morphogenesis of Flaviviruses

Cited by 19 publications

References 119 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

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

St Louis encephalitis virus establishes a productive, cytopathic and persistent infection of Sf9 cells

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