Interaction of Poliovirus with Its Receptor Affords a High Level of Infectivity to the Virion in Poliovirus Infections Mediated by the Fc Receptor

Arita, Minetaro; Horie, Hitoshi; Arita, Masataka; Nomoto, Akio

doi:10.1128/jvi.73.2.1066-1074.1999

Cited by 28 publications

(4 citation statements)

References 53 publications

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“…Poliovirus enters susceptible cells through a specific poliovirus receptor, but can also be taken up by FcγRs (Ref. 164), and FcγRs have been found to be expressed on both microglia and perivascular macrophages (Ref. 165).…”

Section: Fcγrs In Infectionmentioning

confidence: 99%

Low-affinity Fcγ receptors, autoimmunity and infection

Willcocks

Smith

Clatworthy

2009

Expert Rev. Mol. Med.

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Low-affinity Fcgamma receptors (FcgammaRs) mediate the effects of immunoglobulin G (IgG) antibodies on leukocytes, including recruitment to inflammatory lesions, phagocytosis, antibody-dependent cellular cytotoxicity, release of inflammatory mediators and regulation of B cell activation. These functions are an important part of the mammalian response to infection, but if deployed inappropriately can cause autoimmune disease. Although most FcgammaRs are activatory, there is also an inhibitory FcgammaR that, when bound to IgG immune complexes, is able to downregulate the effects of both the activatory FcgammaRs and the B cell receptor. This review discusses the role of the low-affinity FcgammaRs in a balanced immune response and how perturbations in FcgammaR function result in susceptibility to infection or autoimmunity.

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Section: Fcγrs In Infectionmentioning

confidence: 99%

Low-affinity Fcγ receptors, autoimmunity and infection

Willcocks

Smith

Clatworthy

2009

Expert Rev. Mol. Med.

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“…The cells were incubated at 37 uC for 8 h and then fixed with 3 % paraformaldehyde. The cells were stained by indirect immunofluorescence with rabbit hyperimmune serum against the PV 2C protein and Hoechst 33258 (Molecular Probes) for counterstaining (Arita et al, 1999). The numbers of infected cells were counted for the calculation of IU (Jackson et al, 2001).…”

Section: Construction Of An Expression Vector For Pv Capsid Proteinsmentioning

confidence: 99%

Quantitative analysis of poliomyelitis-like paralysis in mice induced by a poliovirus replicon

Arita

Nagata

Sata

et al. 2006

Journal of General Virology

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Poliovirus (PV) infection causes severe paralysis, typically of the legs, by destruction of the motor neurons in the spinal cord. In this study, the relationship between PV replication in the spinal cord, damage in the motor neurons and poliomyelitis-like paralysis was analysed in transgenic mice expressing the human PV receptor (TgPVR21). First, a PV replicon encoding firefly luciferase in place of the capsid genes (PV-Fluc mc) was trans-encapsidated in 293T cells and the trans-encapsidated PV-Fluc mc (TE-PV-Fluc mc) was then inoculated into the spinal cords of TgPVR21 mice. TE-PV-Fluc mc was recovered with a titre of 6?3610 7 infectious units ml "1 , which was comparable to those of PV1 strains. TgPVR21 mice inoculated with TE-PV-Fluc mc showed non-lethal paralysis of the hindlimbs, with severity ranging from a decline in grip strength to complete flaccid paralysis. The replication of TE-PV-Fluc mc in the spinal cord reached peak levels at 10 h post-inoculation (p.i.), followed by the appearance of paralysis at as early as 12 h p.i., reaching a plateau at 16 h p.i. Histological analysis showed a correlation between the lesion and the severity of the clinical symptoms in most mice. However, severe paralysis could also be observed with an apparently low lesion score, where as few as 5?3610 2 motor neurons (1?4 % of the susceptible cells in the lumbar cord) were infected by TE-PV-Fluc mc. These results indicate that PV replication in a small population of the motor neurons was critical for severe residual poliomyelitis-like paralysis in TgPVR21 mice. INTRODUCTIONPoliovirus (PV) is a small, non-enveloped virus with a single-stranded, positive-sense genomic RNA; it is known as the causative agent of poliomyelitis and belongs to the family Picornaviridae. The motor neurons are the major target of PV infection in the central nervous system (CNS) (Bodian, 1949). The tropism of PV to the motor neurons is attributable in part to the expression of the PV receptor (PVR) (Crotty et al., 2002;Ida-Hosonuma et al., 2002;Koike et al., 1994;Ren & Racaniello, 1992).Tissues susceptible to PV infection in the CNS are limited: the brainstem, the roof nuclei of the cerebellum, the precentral gyrus of the cerebrum and the spinal cord (the cervical and lumbar cords) (reviewed by Minor, 1997). Among these tissues in the CNS, the spinal cord seemed to have a high susceptibility to PV infection: PV can adapt to the spinal cord with an increased tropism (Nathanson & Bodian, 1961) and a PV mutant that has a tropism for the spinal cord, but not for the brain, has been isolated (Jia et al., 1999). The adaptation of PV was partly supported by an enhanced efficiency in the uncoating step with decreased thermostability in the virion (Couderc et al., 1996). The lumbar cord supported stable replication of a PV mutant with a severe defect in viral protein synthesis, which showed unstable replication in in vitro-cultured cells and also in the brain (Arita et al., 2004). Experimental infections of other enteroviruses, including coxsackievirus A21 (D...

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“…PVR-IgG2a is a chimeric molecule in which the extracellular moiety of human PVR is joined to the hinge and Fc region of a mouse IgG2a molecule (Arita, Horie, and Nomoto, 1999). Crude PVR-IgG2a was prepared from culture supernatants of recombinant baculovirus-infected Sf9 cells and purified on a protein A-Sepharose 4B column (Pharmacia Biotech) as described (Arita, Horie, and Nomoto, 1999). The concentration of PVR-IgG2a, considered as a dimer like an IgG, was determined by measuring the absorbance at 280 nm.…”

Section: Cells Viruses and Recombinant Pvrmentioning

confidence: 99%

“…Therefore, it is generally believed that the formation of 80S empty capsids results from viral uncoating. PVR-IgG2a (or CD155-IgG2a), a chimeric molecule consisting of an extracellular moiety of PVR and the hinge and Fc portion of a mouse IgG2a, together with Fc receptor-expressing cells, were used to confirm the importance of specific PV-PVR interactions in viral uncoating (Arita, Horie, and Nomoto, 1999). It has also been shown that PVR acts as a catalyst, increasing the rate of capsid transitions by lowering the activation barrier (Tsang et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Characterization of the Poliovirus 147S Particle: New Insights into Poliovirus Uncoating

et al. 2003

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A Sabin 1 strain poliovirus (PV) mutant, S1(2Y-1I), carrying a Tyr at amino acid position VP2(142) and an Ile at position VP1(160), can establish persistent infections in HEp-2c cells. This mutant forms atypical 147S particles upon interaction at 0 degrees C with either cells expressing PV receptor (PVR) CD155, or PVR-IgG2a, a chimeric molecule consisting of an extracellular moiety of PVR and the hinge and Fc portion of a mouse IgG2a. Upon interaction with PVR at 37 degrees C, S1(2Y-1I), similar to the parental strain, forms both 135S A particles and 80S empty capsids. At 0 degrees C, surprisingly, at a concentration equal to or greater than 5 nM, PVR-IgG2a induced both the extrusion of VP4 from the capsid of S1(2Y-1I) and the formation of 80S particles. The same transitions were observed at 0 degrees C with the parental strain Sabin 1 at 40 nM PVR-IgG2a. Thus, the formation of 80S particles and VP4 extrusion, considered as one of the steps of PV uncoating, can be temperature-independent at high PVR concentration. This implies that structural changes of the PV capsid occurred following adsorption at low temperature.

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Interaction of Poliovirus with Its Receptor Affords a High Level of Infectivity to the Virion in Poliovirus Infections Mediated by the Fc Receptor

Cited by 28 publications

References 53 publications

Low-affinity Fcγ receptors, autoimmunity and infection

Low-affinity Fcγ receptors, autoimmunity and infection

Quantitative analysis of poliomyelitis-like paralysis in mice induced by a poliovirus replicon

Characterization of the Poliovirus 147S Particle: New Insights into Poliovirus Uncoating

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