Coxsackievirus B3 adapted to growth in RD cells binds to decay-accelerating factor (CD55)

Bergelson, Jeffrey M.; Mohanty, Joy G.; Crowell, Richard L.; John, Nicole; Lublin, Douglas M.; Finberg, Robert W.

doi:10.1128/jvi.69.3.1903-1906.1995

Cited by 252 publications

(105 citation statements)

References 22 publications

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“…All enteroviruses (including rhinoviruses) have this canyon (78). Although canyons of several enteroviruses function as the receptacle of their respective receptors (e.g., PV, HRV14, and coxsackie B virus 3 [CBV3]), a large number of enteroviruses use structures other than this cleft to attach to the cell (HRV2, some echoviruses, and coxsackie B viruses) (9,(79)(80)(81)(82).…”

Section: Mature Virions: [(Vp4 Vp2 Vp3 Vp1) 5 ] 12 Rnamentioning

confidence: 99%

Picornavirus Morphogenesis

Jiang

Liu

et al. 2014

Microbiol Mol Biol Rev

201

196

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SUMMARY The Picornaviridae represent a large family of small plus-strand RNA viruses that cause a bewildering array of important human and animal diseases. Morphogenesis is the least-understood step in the life cycle of these viruses, and this process is difficult to study because encapsidation is tightly coupled to genome translation and RNA replication. Although the basic steps of assembly have been known for some time, very few details are available about the mechanism and factors that regulate this process. Most of the information available has been derived from studies of enteroviruses, in particular poliovirus, where recent evidence has shown that, surprisingly, the specificity of encapsidation is governed by a viral protein-protein interaction that does not involve an RNA packaging signal. In this review, we make an attempt to summarize what is currently known about the following topics: (i) encapsidation intermediates, (ii) the specificity of encapsidation (iii), viral and cellular factors that are required for encapsidation, (iv) inhibitors of encapsidation, and (v) a model of enterovirus encapsidation. Finally, we compare some features of picornavirus morphogenesis with those of other plus-strand RNA viruses.

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Section: Mature Virions: [(Vp4 Vp2 Vp3 Vp1) 5 ] 12 Rnamentioning

confidence: 99%

Picornavirus Morphogenesis

Jiang

Liu

et al. 2014

Microbiol Mol Biol Rev

201

196

View full text Add to dashboard Cite

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“…Additionally, other viruses use various members of the RAC family as cellular receptors. Epstein-Barr virus, which has also been implicated in MS, uses CD21, while CD55 is used by several echoviruses and coxsackie viruses (Yerfenol et al, 1976;Bergelson et al, 1994Bergelson et al, , 1995. Further studies are needed to determine whether these members of the RAC family that serve as virus receptors play a role in the pathogenesis of MS.…”

Section: E Multiple Infectious "Triggers" In Multiple Sclerosismentioning

confidence: 99%

Role of viruses in etiology and pathogenesis of multiple sclerosis

Soldan

Jacobson

2001

Advances in Virus Research

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“…The exact relationships among these four receptor proteins are still unknown. Although the receptor for CVB3RD has been identified as decaying accelerating factor (DAF) on human cells (Bergelson et al, 1995), the nature of the cellular receptor for other CVB3 strain (CVB3N and CVB3W) remains unclear. Whether the unique heart tropism of CVB3W reflects use of a receptor specificity different from that for CVB3N is unknown.…”

Section: Introductionmentioning

confidence: 99%

Expression and distribution of the receptors for coxsackievirus B3 during fetal development of the Balb/c mouse and of their brain cells in culture

Crowell

1996

Virus Research

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This study was designed mainly to determine the relationships between the expression and distribution of the cellular receptor proteins for coxsackievirus B3 (CVB3) and susceptibility of mouse brain cells during fetal development of Balb/c mice. Immunoblot analysis of fetal extracts demonstrated that the CVB3 receptor proteins were first expressed at day 14 of the fetal stage, and that maximal expression of the cellular receptor occurred at near term or newborn stage. Results also suggested that newborn mouse brain tissue expressed much larger quantities of viral receptor proteins, compared to other tissues. In vitro studies showed that both mouse neurons and astrocytes could be infected by two CVB3 strains, pantropic CVB3 Nancy strain (CVB3N) and myocardiotropic CVB3 Woodruff strain (CVB3W). CVB3N, however, replicated and grew to high titer in primary astrocyte cultures and in primary neuron cultures, whereas, primary astrocyte cultures were relatively resistant to CVB3W. Virus binding assays revealed that CVB3N bound faster and in greater amounts to mouse brain cells than CVBW. These two virus strains, however, were found to share the same receptor specificity by virus competition assays. The number of virus binding sites for CVB3 on newborn mouse brain cells was approximately 1.8 x 10(4) per cell. The data suggested that preferential expression of the cellular receptors on newborn mouse brain cells may be related to their high susceptibilities to CVB3 infection.

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Coxsackievirus B3 adapted to growth in RD cells binds to decay-accelerating factor (CD55)

Cited by 252 publications

References 22 publications

Picornavirus Morphogenesis

Picornavirus Morphogenesis

Role of viruses in etiology and pathogenesis of multiple sclerosis

Expression and distribution of the receptors for coxsackievirus B3 during fetal development of the Balb/c mouse and of their brain cells in culture

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