Measles virus matrix protein detected by immune fluorescence with monoclonal antibodies in the brain of patients with subacute sclerosing panencephalitis

Norrby, Erling; Kristensson, Krister; Brzosko, W. J.; Kapsenberg, Jacoba G.

doi:10.1128/jvi.56.1.337-340.1985

Cited by 52 publications

(13 citation statements)

References 11 publications

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“…Polyclonal anti-MV hyperimmune serum was obtained after immunization of rabbits with purified MV Edmonston grown on Vero cells (21). The preparation and characterization of monoclonal antibodies against MV N and H proteins were described elsewhere (8,10,29). For treatment with antibodies, the medium of semiconfluent cultures was replaced with fresh medium containing anti-MV hyperimmune serum (sufficient to neutralize 104 PFU of MV) or, when indicated, a mixture of neutralizing anti-H antibodies (L77, NC 32, and K83) as a Vol.…”

Section: Materuils and Methodsmentioning

confidence: 99%

Antibody-dependent transcriptional regulation of measles virus in persistently infected neural cells

Schneider‐Schaulies

Liebert

Segev

et al. 1992

J Virol

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Application of neutralizing anti-hemagglutinin antibodies to mouse neuroblastoma cells (NS20Y/MS) persistently infected with measles virus (MV) leads to a significant reduction of viral structural proteins within 6 days. While the transcriptional gradient for MV-specific mRNAs remained unaffected upon antibody treatment, the total amount of MV-specific transcripts dropped by 809% after 24 h. The expression of genomic

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Section: Materuils and Methodsmentioning

confidence: 99%

Antibody-dependent transcriptional regulation of measles virus in persistently infected neural cells

Schneider‐Schaulies

Liebert

Segev

et al. 1992

J Virol

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“…Most of these cell-associated MVs are defective in expression of the matrix (M) protein, which lines the inner surface of the viral envelope (18,61). Moreover, the M protein, as well as the two viral integral membrane proteins, termed fusion (F) protein and hemagglutinin (H) protein, often cannot be detected in brain autopsy material (2,35). Reduced production of the viral envelope proteins in human brain infections can be ascribed partly to a steep gradient of transcription resulting in lowlevel expression of the distally located genes for M, F, and H proteins (9).…”

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confidence: 99%

Cell fusion by the envelope glycoproteins of persistent measles viruses which caused lethal human brain disease

Cattaneo

Rose

1993

J Virol

133

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Measles virus (MV) rarely induces lethal diseases of the human central nervous system characterized by reduced expression of the viral envelope proteins and by lack of viral budding. The MV envelope contains two integral membrane proteins, termed fusion (F) protein and hemagglutinin (H) protein, and a membraneassociated matrix (M) protein. Previously, analysis of MV genes from autopsy material indicated that the M protein and the F protein intracellular domain are often drastically altered by mutations. Here, we present evidence that truncation of the F protein intracellular domain does not impair fusion function, and we suggest that this alteration interferes with viral budding. Unexpectedly, certain combinations of functional F and H proteins were unable to induce syncytium formation, an observation suggesting that specific F-H protein interactions are required for cell fusion. We also found that three of four H proteins of persistent MVs are defective in intracellular transport, oligosaccharide modification, dimerization, and fusion helper function. Thus, MVs replicating in the brain at the terminal stage of infection are typically defective in M protein and in the two integral membrane proteins. Whereas the M protein appears dispensable altogether, partial preservation of F-protein function and H-protein function seems to be required, presumably to allow local cell fusion. Certain subtle alterations of the F and H proteins may be instrumental for disease development.

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“…It was concluded that in SSPE brain, the viral M-protein defect was not a gene deletion, but was rather a block in gene expression. Nonetheless, in some cases of SSPE, M protein was detected in SSPE brain using immunofluorescence and most recently using an extemely sensitive immuno-electron microscope technique [Norrby et al, 1985;Brown et al, 19861. Most previous authors rarely if ever observed viral infection of neurons in PML. Possibly, as in astrocytes, the virus transforms the infected neurons, although the effects of this transformation are not apparent in these mature and nondividing cells.…”

Section: Discussionmentioning

confidence: 99%

Search for virus nucleic acid sequences in postmortem human brain tissue using in situ hybridization technology with cloned probes: Some solutions and results on progressive multifocal leukoencephalopathy and subacute sclerosing panencephalitis tissue

Shapshak

Tourtellotte

Wolman

et al. 1986

J of Neuroscience Research

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In order to obtain a useful and readily applicable in situ hybridization (ISH) protocol for progressive central nervous system (CNS) diseases of unknown etiology that are possibly due to persistent viral infection, known and well described diseases were studied, namely, progressive multifocal leukoencephalopathy (PML) and subacute sclerosing panencephalitis (SSPE). The procedures described were validated by confirming results obtained by other investigators using histology, immunocytochemistry, electron microscopy, and ISH. A number of frequently encountered problems of tissue preparation are addressed as well as techniques to reduce autoradiography exposure times. A multi-staged specific, sensitive, reliable, and valid procedure for detection of viral genomes, mRNA and proteins is approached. Formalin-fixed and paraffin-embedded (FFPE) brain material from six patients who died with PML and one patient who died from SSPE were studied using ISH with a tritium-labeled cloned JC virus DNA probe and a measles-cloned nucleocapsid (NC) gene cDNA probe, respectively. This report constitutes a methodological framework as well as a detailed neuropathological analysis of identified brain cell populations within which in situ hybridization was detected. In early PML lesions, swollen nuclei or oligodendrocytes were the predominant cells labeled, whereas older lesions revealed increased numbers of reactive and bizarre hypertrophic astrocytes hybridized at the outer periphery of the demyelinated lesions. The hybridization varied greatly in intensity in different cells. Intense hybridization was noted very rarely in microglial cells, including rod cells and rarely in venular pericytes, intravascular mononuclear cells, or in vascular endothelial cells. These results, considered together with previous findings, indicate that in PML the viral infection runs different courses in the various cells: in astrocytes the viral genome persists for a long time inducing pathological changes in some cells. In oligodendrocytes the infection rapidly lyses the cells. There was a good correlation between chromatic changes observable in routinely stained sections and virus presence. In addition, in situ hybridization using a measles-NP-cloned probe in white matter from FFPE SSPE brain is presented confirming earlier results in SSPE cryopreserved brain.

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Measles virus matrix protein detected by immune fluorescence with monoclonal antibodies in the brain of patients with subacute sclerosing panencephalitis

Cited by 52 publications

References 11 publications

Antibody-dependent transcriptional regulation of measles virus in persistently infected neural cells

Antibody-dependent transcriptional regulation of measles virus in persistently infected neural cells

Cell fusion by the envelope glycoproteins of persistent measles viruses which caused lethal human brain disease

Search for virus nucleic acid sequences in postmortem human brain tissue using in situ hybridization technology with cloned probes: Some solutions and results on progressive multifocal leukoencephalopathy and subacute sclerosing panencephalitis tissue

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