PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “SSPE Virus”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1989

Long-term effect of elevated temperatures on SSPE virus expression in persistently infected rat glial cells.

Cultivation of measles virus (SSPE virus, Lec strain) persistently infected C6 rat glioma cells at 39 degrees C resulted in the loss of detectable expression of measles virus proteins. Temperature shift-back led to reactivation of measles virus even after maintenance of the cells at 39 degrees C for 15 days. In Northern blot analysis viral mRNA disappeared at 3 days after shift-up whereas 50 S viral genome-sized RNA was detectable until 6 days. The 50 S RNA decreased in quantity in rough correlation with dilution by cell passage at 39 degrees C. The 50 S viral RNA was found in the nucleocapsid fraction. On day 9 after shift-down of persistently infected cells, maintained at 39 degrees C for 15 days, 50 S viral RNA reappeared although mRNAs were not yet detected. Infectious center assays showed that the number of cells in the population at 39 degrees C, which contained an SSPE virus genome that could be reactivated, declined after temperature shift. Moreover, cell cloning experiments, in which single cells of cultures maintained for various lengths of time at 39 degrees C were incubated at 35 degrees C and examined by immunofluorescence, reconfirmed the above results. This indicates that the reactivation of SSPE virus described here was due to re-infection of virus-antigen negative cells with progeny virus produced by a few latently infected cells in the population. The biological significance of this phenomenon in the central nervous system virus infection is discussed.

Animals↗
PubMed1980

Mode of subacute sclerosing panencephalitis (SSPE) virus infection in tissue culture cells. II. Cell-free viruses in cell cultures infected with Kitaken-1 and Biken strains of SSPE virus.

Cell-free infectious viruses were successfully recovered by the aid of freezing and thawing from cultures infected with the Kitaken-1 and Biken strains of subacute sclerosing panencephalitis (SSPE) virus. Our results including those in a previous report which dealt with the Niigata-1 strain of SSPE virus show that cell-free viruses can be detected from all of the SSPE virus-carrying cultures established in Japan. It was also found that cell-free infectious viruses can be recovered efficiently by dispersing the virus-carrying cultures with EDTA. The inclusion of trypsin in the EDTA solution, however, caused a poor recovery of the infectious viruses. Infection of cells with the cell-free viruses readily established the virus-carrying cultures that have characteristics comparable to those of their original cultures. The culture infected with the Kitaken-1 strain produced infectious viruses in about ten times the amount of the other two infected cultures. The buoyant densities of the cell-free infectious viruses were almost the same among the three strains, the values being 1.120 to 1.132, but significantly less than that of 1.164 of measles virus. The low density can be ascribed to one of the characteristics of these SSPE viruses.

Cell Line↗
PubMed1981

Mode of subacute sclerosing panencephalitis (SSPE) virus infection in tissue culture cells. III. Neurovirulence of cell-free SSPE viruses of Niigata-1, Kitaken-1, and Biken strains.

Cell-free viruses recovered from virus-carrying cultures of the Niigata-1, Kitaken-1, and Biken strains of SSPE virus were examined for neurovirulence. The cell-free viruses were prepared by freezing and thawing or by EDTA treatment of the virus-carrying cultures and inoculated into adult mice intracerebrally. A considerable number of the inoculated mice showed clinical signs about 1 to 5 weeks after the inoculation. The first symptom was hyperreactivity, which was followed by paresis and myoclonus. All of the affected mice fell in paralysis and finally died. The virus could be recovered from the moribund mice by cocultivation of the brain cells with Vero cells. Immunofluorescence staining of the brain tissue revealed that infected cells containing viral antigens were distributed sparsely. No inflammatory feature, however, was observed in the brain as far as examined and neutralizing antibody against SSPE virus was not detected in sera from the mice inoculated with the cell-free SSPE viruses.

Animals↗
PubMed1976

The effects of measles virus and various strains of SSPE virus on organotypic cultures of nervous tissue.

The neurotropic effects, virologic behaviors and morphologic appearances of 4 strains of subacute sclerosing panencephalitis (SSPE) virus have been examined in organotypic cultures of hamster cerebellar tissue and have been compared with the Edmonston strain of measles virus in the same system. While measles virus caused extensive damage to nervous tissue, the SSPE strains, in general, exerted a less deleterious effect. All of the SSPE viruses replicated in this tissue. The SSPE strains showed morphologic variation ranging from normal measles-type virions to apparently nucleocapsid deficient forms. It is speculated that some of these differences between measles and SSPE virus may account for the differences in the in vivo conditions with which they are associated.

Animals↗
PubMed1979

Mode of subacute sclerosing panencephalitis (SSPE) virus infection in tissue culture cells. I. Detection of infectious virions from cells infected with Niigata-1 strain of SSPE virus.

By the aid of freezing and thawing, cell-free infectious virions were detected from an apparently nonproductive Vero cell line infected with Niigata-1 strain of subacute sclerosing panencephalitis virus. The production of infectious virions was limited in amount and such virions were detectable only during a limited period after cell subculture. The infectious virions were filtrable through a 0.65 mu membrane filter and neutralized completely by an antiserum against measles virus. The virions were banded at the density of 1.132, while Edmonston strain of measles virus banded at 1.164 in potassium tartrate density gradients. Infectious virions were also released from infected Vero cells by treatment of the cells in a hypotonic solution to an amount comparable to that obtained by freezing and thawing. Infection of normal culture of Vero cells with the infectious virions readily established a virus-cell interaction identical to that in the original infected culture from which the virions were recovered.

Animals↗
PubMed2006

Full-length sequence analysis of subacute sclerosing panencephalitis (SSPE) virus, a mutant of measles virus, isolated from brain tissues of a patient shortly after onset of SSPE.

Subacute sclerosing panencephalitis (SSPE) virus, a measles virus (MeV) mutant, was isolated from brain tissues of a patient shortly after the clinical onset, and the entire viral genome was sequenced. The virus, named SSPE-Kobe-1, formed syncytia on B95a and Vero/SLAM cells without producing cell-free infectious virus particles, which is characteristic of SSPE virus. Phylogenetic analysis classified SSPE-Kobe-1 into genotype D3. When compared with an MeV field isolate of the same genotype (Ich-B strain), SSPE-Kobe-1 exhibited mutation rates of 0.8-1.6% at the nucleotide level in each of the proteincoding regions of the viral genome. It is noteworthy that the mutation rate of the M gene (1.2%) of SSPE-Kobe-1 was considerably lower than for other SSPE virus strains reported so far, but that the majority of the mutations (75%) were the uridine-to-cytidine biased hypermutation characteristic of the SSPE virus M gene. At the amino acid level, the viral proteins, such as N, P, C, V, M, F, H and L proteins, had point-mutations on 3, 7, 1, 4, 3, 9, 8 and 14 residues, respectively, compared with the Ich-B strain. In addition, the F and H proteins had mutated C-termini due to single-point mutations near or at the stop codons. Two of the three mutations in the M protein were Leu-to-Pro mutations, which are likely to affect the conformation and, therefore, the function of the protein. Because of the relatively small number of mutations, SSPE-Kobe-1 would be a useful tool to study genetic evolution of SSPE virus.

Amino Acid Sequence↗
PubMed1976

Growth of measles virus in nervous tissues. IV. Neurovirulence of wild measles and SSPE viruses in monkeys.

Neurovirulence of in vivo-passed wild measles virus and that of the cell-associated SSPE virus were compared by intracerebral inoculation into monkeys. The wild measles virus was found to lack neutrovirulence without producing neurological signs or significant histological changes in the brains, whereas the virus was confirmed to preserve the properties characteristic of the wild virus. In contrast, inoculation of the SSPE virus induced rapid onset of neurological signs with mild but definite histological changes including degeneration of nerve cells. The fact that SSPE virus exhibited neurovirulence in monkeys indicated importance of the current assay system for neurovirulence of measles vaccine by intracerebral inoculation into monkeys.

Animals↗
PubMed1985

Effect of measles virus antibodies on a measles SSPE virus persistently infected C6 rat glioma cell line.

Maintenance of measles (SSPE-Lec) virus persistently infected C6 rat glioma cells in medium containing polyclonal measles antiserum resulted in the loss of detectable expression of all measles virus proteins. Removal of these cells from antiserum, however, led to a re-expression of virus proteins and the production of infectious virus. Cloning of antibody-modulated non-expressing cells in the presence of antiserum showed that re-expression of virus proteins was not due to an incomplete curing process following the addition of antiserum, as a large number of non-expressing cell clones developed the capacity to express measles virus antigen at different periods after removal of antiserum. Irradiation of persistently infected cells to give a non-growing culture showed that modulation was not mediated by a selection and outgrowth of a small percentage of non-expressing cells originally present in the culture. Antibody directed against C6 membrane proteins did not lead to modulation and it was also shown that only monoclonal antibodies with neutralizing activity could affect intracellular antigen expression. Immunoglobulin Fab fragments with neutralizing activity also had modulating activity. Although all modulated cell clones were more susceptible to homologous virus infection than control C6 cells, it was not possible to rescue any defective measles virus which may have been maintained in the culture.

Animals↗
PubMed1988

Effect of interferon on Vero cells persistently infected with Sendai virus compared to Vero cells persistently infected with SSPE virus.

Persistent infections with Sendai and SSPE virus were established in Vero cells. Sequential passages of these cells were monitored by immunofluorescence and for their sensitivity to the antiviral and antiproliferative effects of interferon (IFN). The cells rapidly developed resistance to the antiviral effect of IFN as judged by the inability of IFN to inhibit the replication of exogenous Sindbis virus. This decrease was accompanied by a reduction in the induction of the 2'-5' oligo A synthetase. Both cell lines were resistant to the antiproliferative effect of IFN. A decrease or absence of IFN receptors on the surface of the cells was not found to be the cause of their resistance to IFN.

2',5'-Oligoadenylate Synthetase↗
PubMed2001

Hemadsorption expressed by cloned H genes from subacute sclerosing panencephalitis (SSPE) viruses and their possible progenitor measles viruses isolated in Osaka, Japan.

Most subacute sclerosing panencephalitis (SSPE) viruses, including our Osaka-1, -2, and -3 strains isolated in Osaka, have shown negative hemadsorption (HAD) by African green monkey red blood cells. This property has been thought to be characteristic of SSPE virus as compared to the positive reaction of the standard Edmonston strain of measles virus (MV). However, this assumption has become quite obscure because MV mutates frequently at the genetic level during its multiplication and also because recent field strains isolated by lymphoblastoid cell lines have shown negative HAD. To investigate the above issue, the nucleotide sequences of the hemagglutinin (H) genes from SSPE virus Osaka-1, -2, or -3 strains were compared to those of various MV field strains isolated in Osaka by Vero cells. The H gene sequences of three SSPE strains were relatively conserved without such biased hypermutation as had been observed in the matrix (M) gene of three SSPE strains. However, this analysis of the H gene sequence of the SSPE viruses enabled us to deduce possible progenitor MVs, which are in agreement with the deduction from the M gene analysis we reported previously. The HAD of Vero cells transfected with the cloned H cDNAs from the SSPE strains and their progenitors suggested that negative HAD of the SSPE viruses has been maintained as one of original properties of the progenitor MVs rather than having been acquired as an altered one during long-term persistent infection in the brains of patients with SSPE.

Amino Acid Sequence↗
PubMed1989

Inhibitory effect of selected antiviral compounds on measles (SSPE) virus replication in vitro.

A variety of antiviral compounds were examined for their inhibitory effect on measles (SSPE) virus plaque formation in VERO cells. The following compounds inhibited SSPE virus (strain Niigata-1) replication at concentrations that were significantly lower than their minimum cytotoxic concentrations: neplanocin A, neplanocin C, carbocyclic 3-deazaadenosine, 9-(trans-2', trans-3'-dihydroxycyclopent-4'-enyl)adenine, 9-(trans-2',trans-3'-dihydroxycyclopent-4'-enyl)-3-deazaadenine, (RS)-3-adenin-9-yl-2-hydroxypropanoic acid isobutyl ester, carbodine, cyclopentenyl cytosine, 3-deazaguanine, pyrazofurin, ribavirin and 6-azauridine. As the most selective inhibitors of SSPE virus replication emerged pyrazofurin, 3-deazaguanine, 6-azauridine and ribavirin. These compounds were further examined for their relative potency against a number of measles (SSPE) virus strains. Their order of (decreasing) potency was pyrazofurin greater than 6-azauridine approximately 3-deazaguanine greater than ribavirin. Amantadine, inosiplex and glycyrrhizin, that were also included in these assays, did not show appreciable activity against any of the measles (SSPE) virus strains.

3-Deazauridine↗
PubMed1998

The matrix gene expression of subacute sclerosing panencephalitis (SSPE) virus (Osaka-1 strain): a comparison of two sibling viruses isolated from different lobes of an SSPE brain.

The Fr/V and Oc/V sibling viruses of the Osaka-1 strain of the subacute sclerosing panencephalitis (SSPE) virus were defective in cell-free virus production. By radioimmunoprecipitation assay, the matrix (M) protein was not detected in cells persistently infected with the Osaka-1 strain. This undetectable expression was consistent with the selective reduction of antibody response to the M protein in the patient from whom the Osaka-1 strain was isolated. The sequence of the M gene, however, predicted that the protein could be synthesized because the translational start and stop codons for the protein were not altered. Northern blot hybridization demonstrated the selective defect of the monocistronic mRNAs for the M protein and the phosphoprotein (P) together with the dominant presence of the P-M bicistronic mRNA. This absence of the M mRNA was further confirmed by primer extension analysis. Therefore, the undetectable expression of the M protein in the infected cells was proved to be caused by a transcriptional defect. The two sibling viruses, isolated from remote portions of an SSPE brain, were indistinguishable in their viral characters, including the M gene sequences, which indicates the possibility of clonal expansion of the strain in the brain.

Animals↗
PubMed1986

Effect of interferon on Vero cells persistently infected with SSPE virus and lytically infected with measles virus.

The effect of lymphoblastoid interferon (IFN) on viral polypeptides synthesized in a Vero cell culture persistently infected with subacute sclerosing panencephalitis virus (SSPE-Vero) was compared to that of Vero cells infected with exogenous measles virus. After IFN treatment there was no significant decrease in the synthesis of SSPE viral proteins, but inhibition of synthesis of measles polypeptides was readily seen. In Vero and SSPE-Vero cells IFN was able to inhibit replication of Sindbis virus although the effect in Vero cells was significantly more sensitive. In both cell lines IFN was able to stimulate 2'--5' oligoadenylate synthetase (E enzyme) but not the protein kinase system. The SSPE-Vero cells showed a lower basal level of E enzyme activity than the Vero cells.

2',5'-Oligoadenylate Synthetase↗
PubMed1992

Molecular analysis of virus-producing and non-producing clones derived from a defective SSPE virus Yamagata-1 strain.

Two virus clones were isolated from a defective SSPE virus, the Yamagata-1 strain, and designated as the YA and YF clones. The YA clone-infected cells produced neither cell-free virus nor cell-associated virus, whereas the YF clone-infected cells produced both cell-associated and cell-free virus. No difference of epitopes on structural proteins was observed between these two clones. Both clones had hemadsorption activity. Quantitation of structural protein by Western dot blots showed relatively a lower amount of M protein in the YA-infected cells than that in the YF-infected cells. The ratio, P plus M dicistronic/M monocistronic mRNA, in the YA-infected cells was about twice that in the YF-infected cells. Sequence analysis of cDNA corresponding to P plus M dicistronic mRNA revealed that the deduced M protein of the YF virus was smaller than that of the YA virus by five amino acids from the carboxy terminal. These results suggest that abundant production of P plus M dicistronic mRNA is responsible for the reduced amount of M protein in the non-productive YA clone.

Amino Acid Sequence↗
PubMed2004

Infection of different cell lines of neural origin with subacute sclerosing panencephalitis (SSPE) virus.

Measles virus is the causative agent of subacute sclerosing panencephalitis (SSPE). The viruses isolated from brain cells of patients with SSPE (called SSPE viruses) are defective in cell-free virus production in vitro. To investigate the cell tropism of three strains of SSPE virus (Osaka-1, Osaka-2, Osaka-3), SSPE virus-infected cell cultures were treated with cytochalasin D to prepare virus-like particles (CD-VLPs). All CD-VLPs formed syncytia after infection in CHO cells expressing CD150 but not in those expressing CD46. In addition, an antibody to CD46 did not block the infection of Vero cells by SSPE CDVLPs. The results were consistent with our previous suggestion that one or more unidentified receptors might be involved in the entry process. Infection with the CD-VLPs from three SSPE strains was further examined in different human cell lines, including those of neural origin, and was found to induce syncytia in epithelial cells (HeLa and 293T) as well as neuroblastoma cells (IMR-32 and SK-N-SH) with varying efficiency. SSPE CD-VLPs also infected glioblastoma cells (A172) and astrocytoma cells (U-251) but syncytial formation was rarely induced. These epithelial and neural cell lines were not permissive for the replication of wild-type MV. Together with our previous observations, these results suggest that the cell entry receptor is the major factor determining the cell tropism of SSPE viruses. Further studies are necessary to identify other viral and/or cellular factors that might be involved in the replication of SSPE virus in specific neural cells and in the brain.

Animals↗
PubMed1975

Growth of measles virus in nervous tissues. III. Neurovirulence of SSPE virus in ferrets.

The Niigata-1 strain isolated from a patient with subacute sclerosing panencephalitis (SSPE) was inoculated intracerebrally into ferrets. Neurological signs developed in about 1 week in most of the animals. Histopathological examinations of the central nervous tissues revealed degenerative lesions in the parenchyma of the brains and inflammatory reactions predominantly in the meninges and choroid plexus. Virus antigen was demonstrated mainly in the nerve cells by immunofluorescent staining. The results indicated high affinity of the Niigata-1 strain to the nerve cells. In contrast, the Mantooth strain of SSPE virus in cell-free state did not exhibit neurovirulence in ferrets.

Animals↗