An electron microscopical study of the replication of avirulent Semliki Forest virus in the retina of mice

Pathak, S.; Webb, H. E.

doi:10.1016/0022-510x(88)90038-x

Cited by 9 publications

(4 citation statements)

References 10 publications

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“…Cultured neuroblastoma cells can be productively infected with measles virus in their undifferentiated state, but virus production is significantly reduced on induction of differentiation (Miller and Carrigan, 1982). Similarly, the A7(74) strain of SFV infects and destroys neurons in neonatal and suckling mouse brain but produces nonproductive infection in adult mouse neurons (Pathak et al, 1976;Pathak and Webb, 1988). The same phenomenon may occur when this virus infects oligodendrocytes.…”

Section: B Mechanisms Of Demyelinationmentioning

confidence: 99%

Virus induced demyelination

Fazakerley¹,

Dyson²,

Simas³

1994

Journal of Neuroimmunology

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Section: B Mechanisms Of Demyelinationmentioning

confidence: 99%

Virus induced demyelination

Fazakerley¹,

Dyson²,

Simas³

1994

Journal of Neuroimmunology

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“…It should be noted that the glycoproteins which showed decreased labelling on PID 18 were quite distinct from those which were increased on PID 10. The reduction in transport of glycoproteins cannot have been directly due to the virus itself since replication of SFV within the CNS ceases within a week after SFV inoculation (Illavia et al, 1982;Pathak and Webb, 1988), and is cleared within 12days (Jagelman et al, 1978). It seems more likely that this change was a consequence of demyelination, since myelin loss occurs from PID 14 (Chew-Lim et al, 1977).…”

Section: Changes In Glycoprotein Transport At the Time Of Demyelinationmentioning

confidence: 99%

Changes in Fast Axonal Transport of Glycoproteins in Optic Nerves of Mice Infected With Semliki Forest Virus

1991

Brain

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[ 3 H]fucose incorporation into mouse retinae and subsequent axonal transport of glycoproteins to optic nerve terminals was studied before and during optic nerve demyelination induced by Semliki Forest virus (SFV) infection. As was previously found for [ 3 H]proline-labelled protein, axonally transported glycoprotein was increased before demyelination. Fluorographic analysis of the increased glycoproteins and proteins, after separation by gel electrophoresis, showed particularly large increases in labelling of 2 glycoproteins (38.1 kDa and 45.0 kDa) and 3 protein (15.9 kDa, 23.8 kDa and 27.7 kDa) bands. These increases were due to host-cell rather than viral components. At the time of demyelination, however, [ 3 H]fucose incorporation into retinae of SFV-infected mice was significantly depressed, resulting in reduced label incorporation into axonally transported glycoproteins. Since glycoproteins play a role in axon-glia recognition and adhesion, the early changes in their axonal transport may contribute to the mechanism of demyelination.

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“…The inability of A7 (74) to spread in the brains of 3 ± 4-week-old mice has been linked to a restriction of virus replication which is dependent upon the differentiation state of CNS cells Fazakerley et al, 1993;Oliver et al, 1997;Oliver and Fazakerley, 1998). Despite extensive examination of infected brain tissue under the electron microscope, neither virus particles nor discrete nucleocapsids are observed in CNS cells of adult mice infected with A7(74) (Pathak and Webb, 1988a). Amorphous and ®brous viral material, described as viral core aggregates (VCA), accumulates in isolated CNS cells (Pathak and Webb, 1988b;Fazakerley et al, 1993).…”

Section: Introductionmentioning

confidence: 98%

Aurothiolates enhance the replication of Semliki Forest virus in the CNS and the exocrine pancreas

Scallan

Fazakerley

1999

J Neurovirol

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The A7(74) strain of Semliki Forest virus (SFV) is avirulent and the L10 strain virulent in adult mice. A7(74) infection of adult mouse brain gives rise to small discrete foci of infection which, in immunocompetent animals, are cleared within 10 days. In contrast L10 infection results in a widespread and fatal central nervous system infection. Aurothiolates are linear, 2-coordinate complexes in which two ligands are covalently bound on either side of a gold nucleus in a +1 oxidation state (gold (I)). Pretreatment of A7(74) infected mice with two distinct aurothiolates (sodium aurothiomalate and aurothioglucose) resulted in signi®cantly increased brain virus titers, and large con¯uent areas of infection in the brain similar to the pattern of infection seen with the L10 strain. The gold (I) moiety of aurothiolates was demonstrated to be the active component, since thiomalic acid when administered alone had no potentiating effect on the infection. Although both aurothiolates allowed productive replication and spread of A7 (74) within the nature mouse brain, enhanced neuronal destruction was not apparent. There were no signi®cant changes in virus distribution in any other tissue except for the exocrine pancreas and the myocardium where widespread infection of the acinar cells and occasional infected myocytes were observed.

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An electron microscopical study of the replication of avirulent Semliki Forest virus in the retina of mice

Cited by 9 publications

References 10 publications

Virus induced demyelination

Virus induced demyelination

Changes in Fast Axonal Transport of Glycoproteins in Optic Nerves of Mice Infected With Semliki Forest Virus

Aurothiolates enhance the replication of Semliki Forest virus in the CNS and the exocrine pancreas

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