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PubMed1980

Anesthetic action and virus replication: inhibition of measles virus replication in cells exposed to halothane.

Replication of measles virus in BSC cells was studied in the presence of halothane, a commonly used volatile anesthetic. At clinical concentrations of the anesthetic, appearance of progeny virus was decreased in a dose-related manner. This inhibition was reversible as the removal of halothane allowed virus replication to be resumed. Studies attempting to elucidate the mechanism of action of the anesthetic inhibition of virus replication revealed that halothane did not directly inactivate the virus particle or prevent viral adsorption to the cell. Infectious virus and nucleocapsid production were decreased or stopped, depending on the anesthetic dosage used. Direct immunofluorescent staining for measles virus antigen was negative in cells treated at the higher concentrations of halothane. Recovery of nucleocapsid production started within a few hours after removal of halothane. Furthermore, the combined inhibitory effects on viral ribonucleic acid synthesis of 5-azacytidine and halothane were additive. This evidence suggests that inhibition of measles virus replication occurs at or before ribonucleic acid synthesis.

Anesthesia↗
PubMed1975

Comparative studies on subacute sclerosing panencephalitis virus and a usual measles virus with special reference to their capacities to produce viral hemagglutinin in Vero cells.

Various comparative studies were made on the capacities of a cell-associated subacute sclerosing panencephalitis agent (SSPE agent, Niigata/1 strain) and a usual measles virus (Toyoshima strain) to produce measles virus hemagglutinin (MV-HAnim) in Vero cells. The results obtained by various methods, such as the hemagglutination test (HA), hemadsorption test (HAd), antibody blocking test, antibody inducing test and fluorescent antibody technique (FAT) using monospecific antibody to MV-HAnin, consistently suggested that the SSPE agent was an incomplete measles-like virus having little if any MV-HAnin, but sharing immunologically closely related viral components other than MV-HAnin with those of the usual measles virus. The significance of these findings is discussed with respects to the latency of the SSPE agent.

Animals↗
PubMed1995

Measles virus antisense sequences specifically cure cells persistently infected with measles virus.

Vectors expressing antisense mRNAs complementary to the measles virus (MV) nucleoprotein N or hemagglutinin H genes were used to transfect MV-permissive Vero cells, MV-nonpermissive C6 rat glioma cells, and C6 cells persistently infected with measles/SSPE virus (C6/SSPE cells). Transfected Vero cells infected with MV showed a drastically reduced yield of infectious virus (90-99.99%). In plaque assays, plaque numbers and plaque size were significantly reduced compared with untransfected Vero cells. With an unrelated control virus, VSV, no effects were seen in the transfected Vero cells, underlining the specificity for MV. Following stable transfection with MV antisense vectors, C6 rat glioma cells, which are normally suitable to establish persistently MV-infected lines, can no longer be infected with the virus. In this case also, VSV infection was not influenced. Furthermore, antisense transfection of already persistently infected C6/SSPE cells leads to a loss of MV-specific immunofluorescence, concomitant with a disappearance of viral RNA. Single cell clones from the antisense-transfected C6/SSPE cells appear to be totally free of virus in cocultivation with Vero cells, suggesting that they are really cured. The effectiveness of even low amounts of antisense sequences suggests that they are good candidates for antisense oligonucleotide therapy in tissue culture and might eventually also be useful for in vivo application.

Animals↗
PubMed2002

Importance of the cytoplasmic tails of the measles virus glycoproteins for fusogenic activity and the generation of recombinant measles viruses.

The generation of replication-competent measles virus (MV) depends on the incorporation of biologically active, fusogenic glycoprotein complexes, which are required for attachment and penetration into susceptible host cells and for direct virus spread by cell-to-cell fusion. Whereas multiple studies have analyzed the importance of the ectodomains of the MV glycoproteins hemagglutinin (H) and fusion protein (F), we have investigated the role of the cytoplasmic tails of the F and H proteins for the formation of fusogenic complexes. Deletions in the cytoplasmic tails of transiently expressed MV glycoproteins were found to have varying effects on receptor binding, fusion, or fusion promotion activity. F tail truncation to only three amino acids did not affect fusion capacity. In contrast, truncation of the H cytoplasmic tail was limited. H protein mutants with cytoplasmic tails of <14 residues no longer supported F-mediated cell fusion, predominantly due to a decrease in surface expression and receptor binding. This indicates that a minimal length of the H protein tail of 14 amino acids is required to ensure a threshold local density to have sufficient accumulation of fusogenic H-F complexes. By using reverse genetics, a recombinant MV with an F tail of three amino acids (rMV-FcDelta30), as well as an MV with an H tail of 14 residues (rMV-HcDelta20), could be rescued, whereas generation of viruses with shorter H tails failed. Thus, glycoprotein truncation does not interfere with the successful generation of recombinant MV if fusion competence is maintained.

Amino Acid Sequence↗
PubMed2003

Increased thymic output during acute measles virus infection.

Measles virus infects thymic epithelia, induces a transient lymphopenia, and impairs cell-mediated immunity, but thymic function during measles has not been well characterized. Thirty Zambian children hospitalized with measles were studied at entry, hospital discharge, and at 1-month follow-up and compared to 17 healthy children. During hospitalization, percentages of naïve (CD62L+, CD45RA+) CD4+ and CD8+ T lymphocytes decreased (P = 0.01 for both), and activated (HLA-DR+, CD25+, or CD69+) CD4+ and CD8+ T lymphocytes increased (P = 0.02 and 0.03, respectively). T-cell receptor rearrangement excision circles (TRECs) in measles patients were increased in CD8+ T cells at entry compared to levels at hospital discharge (P = 0.02) and follow-up (P = 0.04). In CD4+ T cells, the increase in TRECS occurred later but was more sustained. At discharge, TRECs in CD4+ T cells (P = 0.05) and circulating levels of interleukin-7 (P = 0.007) were increased compared to control values and remained elevated for 1 month, similar to observations in two measles virus-infected rhesus monkeys. These findings suggest that a decrease in thymic output is not the cause of the lymphopenia and depressed cellular immunity associated with measles.

Acute Disease↗
PubMed1980

[Studies on establishment and maintenance of persistent infection with measles virus in NC-37 cell. II. Effect of DNA-synthesis-suppressing factor (DSF) on the production of interferon in NC-37 cell infected with measles virus (author's transl)].

The attenuated strain of measles viruses, Schwarz, CAM-70, or subacute sclerosing panencephalitis (SSPE) virus of measles viruses, Halle, Mantooth was good interferon inducer, but the virulent strain, Edmonston, Toyoshima induced few amount of interferon or not. Furthermore, an inverse relationship seemed to exist between the ability to induce interferon and DNA synthesis suppressing factor (DSF). The attenuated strain or SSPE virus which had not a capacity to produce DSF could induce interferon and establish persistent infection in human lymphoid cell NC-37, while virulent strain did not induce interferon but DSF. Maximum yield of progeny virus was precede the detection of interferon in culture fluids. A persistently infected cells also produced continuously interferon and progeny virus. It is demonstrated that DSF suppressed interferon production by infection of measles virus and that DSF had not an activity like interferon.

Cells, Cultured↗
PubMed1979

Heterogeneity of virus particles in measles virus.

A heterogeneous population of virions is generated by measles virus-infected cells. These particles are partially separable by sucrose density centrifugation into three peaks. Each population is stable and contains infectious particles. The particles of all three populations contain at least six polypeptide species that differ between particle populations only in quantity. All three populations contain a 50S RNA species, and the heaviest density peak also contains an additional species of 43S RNA. The difference between these results and previous studies with measles virions will be discussed.

Animals↗
PubMed2001

Vaccination with recombinant modified vaccinia virus Ankara protects against measles virus infection in the mouse and cotton rat model.

Modified vaccinia virus Ankara (MVA) has been used as an experimental vaccine vector against respiratory infections. We have tested the safety and immunogenicity of a recombinant virus expressing the hemagglutinin of measles virus (MVA-MV-H) using the mouse model of measles virus induced encephalitis and the cotton rat model for respiratory infection. MVA-MV-H proved to induce a TH1 response, neutralizing antibodies and conferred protection against both encephalitis and lung infection. The cotton rat is very sensitive to infection with replication competent vaccinia virus. In these animals MVA-MV-H proved to be a very well tolerated vaccine. However, the efficiency in the presence of MV specific maternal antibodies was low (even using a prime-boost strategy) and therefore might have to be improved.

Animals↗
PubMed2002

Genetic homogeneity of measles viruses associated with a measles outbreak, São Paulo, Brazil, 1997.

During a resurgence of measles in São Paulo, Brazil, in 1997, >40,000 cases (peak incidence rate of 246/100,000 inhabitants) and 42 measles-related deaths were reported. Reverse transcriptase-polymerase chain reaction and nucleotide sequencing were used to analyze specimens from patients who had typical clinical measles infection during this outbreak and from six patients who had had measles in 1995 and 1996. Although wild-type measles viruses (genotypes D5 and D6) were present in São Paulo before this resurgence, we detected only D6 viruses. The genotype D6 viruses isolated during this outbreak had identical sequences to genotype D6 viruses isolated in other parts of Brazil and South America in 1997 and 1998, suggesting that a single chain of transmission was responsible. We also identified genotype A viruses in two vaccine-associated cases from 1995 and 1996. Our findings extend the knowledge of the circulation patterns of measles virus in South America, contributing to measles control efforts in the Americas.

Brazil↗
PubMed2000

Transgenic mice expressing human HLA and CD8 molecules generate HLA-restricted measles virus cytotoxic T lymphocytes of the same specificity as humans with natural measles virus infection.

Control of primary measles virus (MV) infection in humans and continued maintenance of immune memory that protects against reinfection are mediated primarily through the anti-MV T cell response, as judged by observations of children with defects in antibody formation but competency in making T cells. Further, the failure of T cell responses in those infected with MV most often leads to overwhelming infection. To better define and manipulate the elements involved in human T cell responses to MV, we analyzed the generation of HLA-restricted cytotoxic T lymphocytes (CTL) in a small animal model. Transgenic mice expressing the human class I MHC antigen HLA-B27 in conjunction with human CD8 molecules produced vigorous HLA-restricted CTL responses to MV antigens, paralleling those in MV infection of humans. In addition, such humanized mice generated human CD8 coreceptor-dependent HLA-B27-restricted CTL with the same specificity for recognition of MV fusion (F) peptide RRYPDAVYL as reported for humans during natural MV infection. Neither murine beta(2)-microglobulin nor murine CD8 substituted adequately as coreceptors for the HLA-B27 heavy chain. By contrast, HLA-A2.1-restricted responses to measles could be generated in the absence of expression of human beta(2)-microglobulin or CD8(+) molecules in HLA-A2.1/K(b) transgenic mice. Thus a small animal model is now available for studying strategies for optimizing human CD8(+) T cell responses and for testing vaccines. This model offers the potential, when combined with the newly reported CD46 transgenic mouse model in which MV replicates in cells of the immune system, for uncoding the molecular mechanism of MV-induced immunosuppression.

Animals↗
PubMed2006

Nonpeptide inhibitors of measles virus entry.

Measles virus (MV) is one of the most infectious pathogens known. Despite the existence of a vaccine, over 500,000 deaths/year result from MV or associated complications. Anti-measles compounds could conceivably reverse these statistics. Previously, we described a homology model of the MV fusion protein trimer and a putative binding site near the head-neck region. The resulting model permitted the identification of two nonpeptidic entry inhibitors. Here, we present the design, synthesis, and bioevaluation of several series of fusion inhibitors and describe their structure-activity relationships (SAR). Five simply substituted anilides show low-microM blockade of the MV, one of which (AS-48) exhibits IC50 = 0.6-3.0 microM across a panel of wild-type MV strains found in the field. Molecular field topology analysis (MFTA), a 2D QSAR approach based on local molecular properties (atomic charges, hydrogen-bonding capacity and local lipophilicity), applied to the anilide series suggests structural modifications to improve potency.

Anilides↗
PubMedDate not supplied

Genetic diversity of wild-type measles viruses: implications for global measles elimination programs.

Wild-type measles viruses have been divided into distinct genetic groups according to the nucleotide sequences of their hemagglutinin and nucleoprotein genes. Most genetic groups have worldwide distribution; however, at least two of the groups appear to have a more limited circulation. To monitor the transmission pathways of measles virus, we observed the geographic distribution of genetic groups, as well as changes in them in a particular region over time. We found evidence of interruption of indigenous transmission of measles in the United States after 1993 and identified the sources of imported virus associated with cases and outbreaks after 1993. The pattern of measles genetic groups provided a means to describe measles outbreaks and assess the extent of virus circulation in a given area. We expect that molecular epidemiologic studies will become a powerful tool for evaluating strategies to control, eliminate, and eventually eradicate measles.

Genetic Variation↗
PubMed1999

Pathogenic aspects of measles virus infections.

Measles virus (MV) infections normally cause an acute self limiting disease which is resumed by a virus-specific immune response and leads to the establishment of a lifelong immunity. Complications associated with acute measles can, on rare occasions, involve the central nervous system (CNS). These are postinfectious measles encephalitis which develops soon after infection, and, months to years after the acute disease, measles inclusion body encephalitis (MIBE) and subacute sclerosing panencephalitis (SSPE) which are based on a persistent MV infection of brain cells. Before the advent of HIV, SSPE was the best studied slow viral infection of the CNS, and particular restrictions of MV gene expression as well as MV interactions with neural cells have revealed important insights into the pathogenesis of persistent viral CNS infections. MV CNS complication do, however, not large contribute to the high rate of mortality seen in association with acute measles worldwide. The latter is due to a virus-induced suppression of immune functions which favors the establishment of opportunistic infections. Mechanisms underlying MV-mediated immunosuppression are not well understood. Recent studies have indicated that MV-induced disruption of immune functions may be multifactorial including the interference with cytokine synthesis, the induction of soluble inhibitory factors or apoptosis and negative signalling to T cells by the viral glycoproteins expressed on the surface of infected cells, particularly dendritic cells.

Animals↗
PubMed1986

Characterization of epitopes on the measles virus hemagglutinin.

Measles virus hemagglutinin epitopes were analyzed using nine monoclonal antibodies (MAbs) in competitive binding assays (CBA) and by in vitro selection of antigenic variants. In CBA the nine MAbs formed four different but partially overlapping binding groups. In vitro selected variants were analyzed by radioimmune precipitation assay, hemagglutination inhibition (HI), and neutralization assays. Seven operationally distinct MAb antigenic sites could be delineated: two sites were defined by two MAbs to each and five sites by single MAbs. Variants which had lost reactivity to different combinations of MAbs were generated by a branched sequential selection procedure. The most epitopically modified variants had lost reactivity in all assays to eight MAbs. None of these variants showed any major changes in hemagglutination nor neurotropism per se. Only minor changes were detected by HI in reactivity of these variants with human measles antiserum indicating that the epitopic changes were not of major epidemiological significance at least in terms of HI.

Antibodies, Monoclonal↗
PubMed1992

Expression and properties of the V protein in acute measles virus and subacute sclerosing panencephalitis virus strains.

Measles virus (MV) inserts one guanosine (G) residue at a specific site in a subpopulation of the mRNA transcribed from the phosphoprotein (P) gene to produce V mRNA. Using an antiserum against the unique carboxyl-terminal region of the predicted V protein, we found that a phosphorylated V protein was expressed in two acute MV strains (Edmonston and Nagahata) and three SSPE virus strains (Biken, Yamagata, and Niigata). The V protein of Biken strain SSPE virus was electrophoretically and antigenically indistinguishable from the V protein of Nagahata strain acute MV, the likely progenitor of the Biken strain. The V protein of these two viruses was not present in the intracellular viral nucleocapsids, but was found only in the cytosolic free protein pool. Pulse-chase experiments failed to show transport of the V protein to the plasma membrane. The V protein was also absent in the extracellular virions. The P protein synthesized from the cloned gene associated with the MV nucleocapsids in vitro, but the V protein had no affinity to the MV nucleocapsids. These results suggest that expression and properties of the V protein are conserved in chronic MV infection.

Animals↗
PubMed1988

Comparative clinico-morphological investigations of the CNS of monkeys and of the eye teguments of guinea pigs infected with different measles virus strains.

Measles virus strains Edmonston and L-16 have been studied in 10 intracerebrally (i.c.) infected monkeys and in 155 guinea pigs infected into the anterior eye chamber. The strains appeared to differ in pathogenicity for monkeys and guinea pigs. The more pathogenic Edmonston strain caused encephalitis in monkeys, whereas in guinea pigs it caused iridocyclitis, keratoconjunctivitis and follicular conjunctivitis. Strain L-16 was not neurovirulent for monkeys, while in guinea pigs it caused follicular conjunctivitis. Specific pathohistological changes detected in the CNS of monkeys and in the eye teguments of guinea pigs were confirmed by virologic and serologic findings.

Animals↗
PubMed1987

Induction of class I and class II transplantation antigens in rat brain during fatal and non-fatal measles virus infection.

Measles virus induced a marked increase in the expression of MHC-coded class I and class II antigens as detected by immunostaining during both fatal and non-fatal brain infections in rats. The distribution of these molecules in the brain was much more widespread than the occurrence of viral antigen suggesting a soluble factor for their induction. In 14-day-old rats with a non-fatal infection there was a marked infiltration of T lymphocytes of 'cytotoxic/suppressor' phenotype in the brain parenchyma, whereas T 'helper' cell phenotypes mainly were located perivascularly. In brains from newborn rats with a fatal infection no or only few lymphocytes were detected.

Animals↗