Comparison of the binding characteristics to BHK-21 cells of viruses representing the two Theiler's virus neurovirulence groups

Fotiadis, Chris; Kilpatrick, David R.; Lipton, Howard L.

doi:10.1016/0042-6822(91)90683-3

Cited by 39 publications

(52 citation statements)

References 24 publications

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“…The TMEV strain GDVII was not used in this study due to its ability to infect BW cells at low as well as high MOIs. This is in contrast to the nding by Fotiadis et al (1991) that GDVII does not productively infect BW. We assayed for the presence of the constitutive, mammalian expression vector constructed to express the P0 cDNA product, P0/pRc-CMV#4, after transfection into BW cells and selection via PCR on plasmid samples prepared from the transfected cells.…”

Section: Sequence Comparisoncontrasting

confidence: 53%

“…BW cells are not infected by DA virus at low MOI but can be infected at much higher MOI (Fotiadis et al, 1991;Kilpatrick and Lipton, 1991;McCright and Fujinami, 1997). This infectivity may be due to the presence of an inef cient and/or low abundance receptor on the BW cells.…”

Section: Have Reported That Schwann Cells Are Susceptible To Da Virusmentioning

confidence: 99%

“…Expression of P0 protein in BW5147.G.1.4 cells BW cells were selected for this study based on their inability to be infected by DA virus at low multiplicity of infection (MOI) and their ability to support viral replication upon infection at much higher MOI or upon transfection with viral RNA (Fotiadis et al, 1991;Kilpatrick and Lipton, 1991;McCright and Fujinami, 1997). The TMEV strain GDVII was not used in this study due to its ability to infect BW cells at low as well as high MOIs.…”

Section: Sequence Comparisonmentioning

confidence: 99%

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Peripheral nerve protein, P0, as a potential receptor for Theiler's murine encephalomyelitis virus

et al. 2001

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Section: Sequence Comparisoncontrasting

confidence: 53%

Section: Have Reported That Schwann Cells Are Susceptible To Da Virusmentioning

confidence: 99%

Section: Sequence Comparisonmentioning

confidence: 99%

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Peripheral nerve protein, P0, as a potential receptor for Theiler's murine encephalomyelitis virus

et al. 2001

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“…Recently, PML has also been reported in patients being treated with Natalizumab, a drug designed to inhibit leukocyte trafficking into inflamed tissue (Kleinschmidt-DeMasters and Tyler, 2005;Langer-Gould et al, 2005;Van Assche et al, 2005). PML is thought to develop following reactivation of the virus and dissemination from peripheral sites to the CNS, where the primary targets are astrocytes and oligodendrocytes (Achim and Wiley, 1992;Fotiadis, Kilpatrick, and Lipton, 1991;Telenti et al, 1992). Others have suggested that reactivation of latent JCV within the CNS can also contribute to the development and progression of PML (Boone et al, 1992;Elsner and Dorries, 1992;Kestler Harry et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Interferon β1-a and selective anti-5HT2a receptor antagonists inhibit infection of human glial cells by JC virus

O’Hara

Atwood

2008

Virus Research

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JC virus (JCV) is the causative agent of progressive multifocal leukoenchaphalopathy (PML). The disease develops when JCV gains access to the central nervous system, infects and destroys oligodendrocytes. The disease is rapidly progressing, typically fatal and no effective therapies exist to treat or prevent PML. The recent occurrence of PML in multiple sclerosis patients being treated with Avonex (IFNβ1a) and Tysabri (Natalizumab) and the recent reports linking JCV infection to the 5HT 2a serotonin receptor led us to evaluate the effects of IFNβ1-a and a panel of 5HT 2a receptor antagonists for their ability to modulate virus infection. IFNβ1-a was found to be a potent inhibitor of both virus infection and viral early and late gene expression. In addition, several 5HT 2a receptor antagonists inhibited initial infection of cells by JCV but were less effective and reducing viral loads in an already established infection.

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“…Efforts to identify the host receptor for Theiler's virus have been reported (9). When membrane proteins of susceptible cells were separated by gel electrophoresis, radiolabeled TMEV was found to bind predominantly to a 34-kDa glycoprotein (20).…”

mentioning

confidence: 99%

Sialylation of the Host Receptor May Modulate Entry of Demyelinating Persistent Theiler's Virus

Zhou

Luo

Wu³

et al. 2000

J Virol

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Theiler's murine encephalomyelitis virus (TMEV) is a picornavirus of the Cardiovirus genus. Certain strains of TMEV may cause a chronic demyelinating disease, which is very similar to multiple sclerosis in humans, associated with a persistent viral infection in the mouse central nervous system (CNS). Other strains of TMEV only cause an acute infection without persistence in the CNS. It has been shown that sialic acid is a receptor moiety only for the persistent TMEV strains and not for the nonpersistent strains. We report the effect of sialylation on cell surface on entry and the complex structure of DA virus, a persistent TMEV, and the receptor moiety mimic, sialyllactose, refined to a resolution of 3.0 Å. The ligand binds to a pocket on the viral surface, composed mainly of the amino acid residues from capsid protein VP2 puff B, in the vicinity of the VP1 loop and VP3 C terminus. The interaction of the receptor moiety with the persistent DA strain provides new understanding for the demyelinating persistent infection in the mouse CNS by TMEV.Theiler's murine encephalomyelitis virus (TMEV) belongs to the Cardiovirus genus of the family Picornaviridae based on sequence analysis (34). Based on the characteristics of the disease they cause, TMEV strains are divided into two groups. Viruses of one group, including strain GDVII and FA, are highly neurovirulent, causing a rapid destruction of the neuron and killing their host in a matter of days. These viruses are unable to persist and to induce demyelination in those rare survivors (22). The other group, including strains DA, BeAn, WW, TO4, and Yale, are referred to as the Theiler's original (TO) group (23). Viruses of the TO group are much less virulent than GDVII and FA and cause a biphasic disease with mild central nervous system (CNS) damage. The first phase, or early onset, is acute encephalitis that occurs during the initial few days following intracranial inoculation. At that time, the virus is also found in neurons of the gray matter in the brain and spinal cord. However, the number of infected cells is small and most of the animals survive. Soon after, the neurons are cleared of the virus and the disease enters a second phase, or late onset, during which the virus is found to be persistent in the white matter of the spinal cord. At this stage of the viral persistence, patchy inflammation and demyelination develops in the spinal cord at the sites of infection (7, 23). The symptoms of the demyelination disease of mice caused by TMEV persistence infection in the CNS resemble those of multiple sclerosis (MS), a chronic demyelinating disease of the human CNS. Among the animal models of virus-induced demyelination in the last two decades, TMEV infection has emerged as one of the best models for studying MS.Although these two groups of TMEV strains have both been shown to replicate well in BHK-21 cells and share high amino acid sequence homology (31, 34-36), they apparently display different pathogenesis characteristics in vivo. Many efforts have been taken to map ...

show abstract

Comparison of the binding characteristics to BHK-21 cells of viruses representing the two Theiler's virus neurovirulence groups

Cited by 39 publications

References 24 publications

Peripheral nerve protein, P0, as a potential receptor for Theiler's murine encephalomyelitis virus

Peripheral nerve protein, P0, as a potential receptor for Theiler's murine encephalomyelitis virus

Interferon β1-a and selective anti-5HT2a receptor antagonists inhibit infection of human glial cells by JC virus

Sialylation of the Host Receptor May Modulate Entry of Demyelinating Persistent Theiler's Virus

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