Two mutations in the envelope glycoprotein E2 of semliki forest virus affecting the maturation and entry patterns of the virus alter pathogenicity for mice

Glasgow, Gwendoline M.; Sheahan, B. J.; Atkins, Gregory J.; Wahlberg, J M; Salminen, Antti; Lilieström, Peter

doi:10.1016/0042-6822(91)90545-m

Cited by 53 publications

(60 citation statements)

References 42 publications

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“…Virulent strains such as the prototype strain or the L10 strain cause a lethal threshold of damage to neurons in the CNS (Atkins & Sheahan, 1982 ;Atkins et al, 1990 ;Smyth et al, 1990 ;Glasgow et al, 1991 ;Balluz et al, 1993). Avirulent strains or mutants such as A7 and M9 are less cytopathic for neurons (Atkins et al, 1985(Atkins et al, , 1995Fazakerley et al, 1993) and induce demyelination which is triggered by infection of oligodendrocytes (Atkins et al, 1985(Atkins et al, , 1994 and is partially immune-mediated (Gates et al, 1984 ;Fazakerley & Webb, 1987 ;Subak-Sharpe et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

“…This clone was constructed from the prototype strain of SFV of known sequence (Garoff et al, 1980 a, b ;Takkinen, 1986). On transcription and electroporation into BHK cells it produces SFV4 virus, which is virulent when given intranasally (Glasgow et al, 1991). In order to identify pathogenicity determinants of the A7 strain of SFV, we sequenced the envelope protein region and showed that A7 differed from SFV4 in amino acid sequence.…”

Section: Introductionmentioning

confidence: 99%

“…1 ; Liljestro$ m et al, 1991 ;Glasgow et al, 1991Glasgow et al, , 1994Santagati et al, 1995). This clone was constructed from the prototype strain of SFV of known sequence (Garoff et al, 1980 a, b ;Takkinen, 1986).…”

Section: Introductionmentioning

confidence: 99%

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Sequence analysis of the avirulent, demyelinating A7 strain of Semliki Forest virus.

Tarbatt

Glasgow

Mooney

et al. 1997

Journal of General Virology

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The nonstructural region of the genome of the avirulent A7 strain of Semliki Forest virus (SFV) has been sequenced, so that the complete nucleotide sequence is available. Compared to the virulent SFV4 strain (produced from the infectious clone pSP6-SFV4), A7 contains 226 nucleotide changes in the translated region, which result in 47 amino acid changes. The 5h nontranslated region has two nucleotide changes, and the 3h nontranslated region is longer in A7 than SFV4, and contains divergent

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Sequence analysis of the avirulent, demyelinating A7 strain of Semliki Forest virus.

Tarbatt

Glasgow

Mooney

et al. 1997

Journal of General Virology

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“…Further studies are necessary of infected animals before cell death mechanisms in cell culture can be confirmed in animals. However, it is clear that the cell culture systems described in this and previous studies, together with the availability of an infectious clone of SFV (Glasgow et al, 1991), represent a potential model system for molecular analysis of viral and cellular processes leading to cell death. …”

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confidence: 99%

“…The virulent SFV4 strain of SFV, derived from an infectious clone (Glasgow et al, 1991), and the avirulent A7 strain of SFV were grown and plaque assayed using BHK-21 cells, as previously described (Balluz et al, 1993). Neuron and glial cell cultures were prepared from neonatal rat brain as previously described ( Gates et al, 1985 ;Atkins et al, 1990) ; neurons are 95 % pure and do not proliferate, whereas glial cells consist mainly of a mixture of proliferating oligodendrocytes and astrocytes (Walker et al, 1984).…”

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confidence: 99%

Death mechanisms in cultured cells infected by Semliki Forest virus.

Glasgow

McGee

Sheahan

et al. 1997

Journal of General Virology

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We have investigated the induction of cell death in cultured cells by the virulent SFV4 and avirulent A7 strains of Semliki Forest virus (SFV). In BHK cells, death occurred by a typical apoptotic mechanism, as did the death of oligodendrocytes in glial cell cultures. For cerebellar neuron cultures, virusinduced death was due to necrosis. Although the SFV4 and A7 strains did not differ in the mechanism of induction of cell death, the virulent SFV4 strain did multiply to a higher titre in cultured neurons than the avirulent A7 strain. This is consistent with previous animal studies which indicate that the virulence of SFV strains is controlled by rapidity of multiplication in the CNS, leading to a lethal threshold of damage, rather than differential cell tropism or cell death mechanisms. The immunemediated demyelination induced by avirulent strains may be triggered by apoptosis of oligodendrocytes, the consequences of which are obscured by death for virulent strains.Cell death mechanisms are an important component of pathogenesis in virus infections, although the mechanisms of induction of cell death are not well understood. The fate of infected cells, especially cells of the central nervous system (CNS), is of critical importance to mortality and morbidity in virus disease. A number of animal models of virus neuropathogenesis have been investigated in an attempt to define events which determine virulence (Atkins et al., 1994).One such model is infection of mice and rats by the alphavirus Semliki Forest virus (SFV ; Atkins et al., 1985). SFV causes fatal encephalitis following infection by virulent strains and immune-mediated demyelination following infection by avirulent strains. Virulent strains grow to high titre in the CNS and induce fatal damage to neurons. In contrast, avirulent strains multiply slowly, causing less neuronal damage, and are cleared from the CNS by immune intervention (Atkins &

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Expression of heterologous proteins in cultured rat hippocampal neurons using the semliki forest virus vector

Olkkonen

Liljeström

Garoff

et al. 1993

J of Neuroscience Research

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The Semliki Forest virus expression vector (Liljeström and Garoff: Bio/Technology 9:1356-1361, 1991) was tested in cultured rat hippocampal neurons using two Madin-Darby canine kidney (MDCK) cell membrane-associated proteins as reporters: rab8, a small GTPase involved in post-Golgi vesicle transport, and VIP21, an integral membrane protein of caveolae, trans-Golgi network, and post-Golgi vesicles. Expression of the c-myc epitope-tagged proteins was visualized by immunofluorescence microscopy. The proteins were first detected in neurons after 3-4 hr infection by the recombinant viruses. The infection efficiency on neurons was high: after 6 hr infection at a multiplicity of one, 50-60% of the cells expressed the reporter proteins. The neurons tolerated the infection well up to 8 hr. Their polarized organization was not disturbed, as judged from morphology and from distribution of the dendritic MAP2 and axonal synaptophysin marker proteins. The Semliki Forest virus vector thus seems suitable for short-term expression of proteins in cultured neurons.

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Two mutations in the envelope glycoprotein E2 of semliki forest virus affecting the maturation and entry patterns of the virus alter pathogenicity for mice

Cited by 53 publications

References 42 publications

Sequence analysis of the avirulent, demyelinating A7 strain of Semliki Forest virus.

Sequence analysis of the avirulent, demyelinating A7 strain of Semliki Forest virus.

Death mechanisms in cultured cells infected by Semliki Forest virus.

Expression of heterologous proteins in cultured rat hippocampal neurons using the semliki forest virus vector

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