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PubMedDate not supplied

[Immunizing and immunomodulating activity of wild measles virus at the focus of measles infection].

The effect of a wild measles virus circulating in a childhood collective body on the immune status of 80 children has been studied over time. Only using enzyme immunoassay was it possible to fully record and assess the degree of booster effect of the virus on children in case of infection transmission. In 25% cases the increment of antibodies was at the expense of specific IgM antibodies appearing in the sera of children. By the end of the first month 60% of children developed a relative measles immunodepression. Analysis of the index of cell stimulation with phytohemagglutinin in the presence of suppressors enabled us to single out a group of children (30%) with weakly expressed suppressive factor. The observed phenomenon with a high degree of reliability may be used as an index of immune response development.

Child↗
PubMed1989

Characterization of a halothane-resistant strain of measles virus.

A strain of measles virus (MVr) whose replication demonstrated increased resistance to halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) exposure compared with the susceptible parental strain (MVs) is described. After exposure to a 1.2% halothane concentration, substantial amounts of the measles virus H protein were detected in MVr-infected Vero cell lysates by immunoprecipitation and polyacrylamide gel electrophoresis or by quantitative immunofluorescence staining. The protein was barely detectable in identically treated MVs-infected lysates, however. The recovery of all other measles virus proteins studied was the same in MVr- and MVs-infected cells at this anesthetic concentration. Thus, the altered expression of a single gene product appears to be responsible for the observed halothane resistance.

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↗
PubMed2005

Rab9 GTPase is required for replication of human immunodeficiency virus type 1, filoviruses, and measles virus.

Rab proteins and their effectors facilitate vesicular transport by tethering donor vesicles to their respective target membranes. By using gene trap insertional mutagenesis, we identified Rab9, which mediates late-endosome-to-trans-Golgi-network trafficking, among several candidate host genes whose disruption allowed the survival of Marburg virus-infected cells, suggesting that Rab9 is utilized in Marburg replication. Although Rab9 has not been implicated in human immunodeficiency virus (HIV) replication, previous reports suggested that the late endosome is an initiation site for HIV assembly and that TIP47-dependent trafficking out of the late endosome to the trans-Golgi network facilitates the sorting of HIV Env into virions budding at the plasma membrane. We examined the role of Rab9 in the life cycles of HIV and several unrelated viruses, using small interfering RNA (siRNA) to silence Rab9 expression before viral infection. Silencing Rab9 expression dramatically inhibited HIV replication, as did silencing the host genes encoding TIP47, p40, and PIKfyve, which also facilitate late-endosome-to-trans-Golgi vesicular transport. In addition, silencing studies revealed that HIV replication was dependent on the expression of Rab11A, which mediates trans-Golgi-to-plasma-membrane transport, and that increased HIV Gag was sequestered in a CD63+ endocytic compartment in a cell line stably expressing Rab9 siRNA. Replication of the enveloped Ebola, Marburg, and measles viruses was inhibited with Rab9 siRNA, although the non-enveloped reovirus was insensitive to Rab9 silencing. These results suggest that Rab9 is an important cellular target for inhibiting diverse viruses and help to define a late-endosome-to-plasma-membrane vesicular transport pathway important in viral assembly.

Animals↗
PubMedDate not supplied

The cellular receptor for measles virus--elusive no more.

The identity of the measles virus receptor has been controversial. Several years ago CD46 was identified as a cellular receptor for the Edmonston strain of measles virus, but most clinical isolates of measles virus, which are most efficiently isolated in the marmoset B cell line B95a, cannot grow in many CD46+ cell lines. Although some researchers attributed it to post-entry block in viral replication, others believed that there is a receptor other than CD46 for wild-type measles viruses. A new study showed that human signalling lymphocytic activation molecule (SLAM; also known as CDw150) is a cellular receptor for measles virus, including the Edmonston strain. SLAM is expressed on lymphocytes and dendritic cells, and plays an important role in lymphocyte activation. The identification of SLAM as a measles virus receptor nicely explains the pathogenesis of measles virus infection.

Antigens, CD↗
PubMed1984

Viruses disrupt functions of human lymphocytes. Effects of measles virus and influenza virus on lymphocyte-mediated killing and antibody production.

We present experimental data that offer, in part, a better understanding of the immunosuppression that accompanies measles virus infection. We note that measles virus "silently" infects human lymphocytes and that the infection does not alter lymphocyte survival in vitro. Yet such infected lymphocytes fail to generate natural killer (NK) cell activity or synthesize immunoglobulins (Ig). Thus, the presence of virus within lymphocytes impairs their specific immune functions in the absence of cytolysis. Influenza virus also infects human lymphocytes. In contrast to measles virus infection of resting lymphocytes in which viral antigen is rarely expressed, influenza virus infection of these cells yields viral antigens expressed in the cytoplasm and on the cell surface. Influenza virus-infected lymphocytes have normal NK cell activity but fail to synthesize IgG or IgM.

Adult↗
PubMed2004

The phosphoprotein (P) and L binding sites reside in the N-terminus of the L subunit of the measles virus RNA polymerase.

Measles virus encodes an RNA-dependent RNA polymerase composed of the L and P proteins. Recent studies have shown that the L proteins of both Sendai virus and parainfluenza virus 3 form an L-L complex [Cevik, B., Smallwood, S., Moyer, S.A., 2003. The oligomerization domain resides at the very Nterminus of the Sendai virus L RNA polymerase protein. Virology 313, 525-536.; Smallwood, S., Moyer, S.A., 2004. The L polymerase protein of parainfluenza virus 3 forms anoligomer and can interact with the heterologous Sendai virus L, P and C proteins. Virology 318, 439-450.; Smallwood, S., Cevik, B., Moyer, S.A., 2002. Intragenic complementation and oligomerization of the L subunit of the Sendai virus RNA polymerase. Virology 304, 235-245.]. Using differentially tagged L proteins, we show here that measles L also forms an oligomer and the L-L binding site resides in the N-terminal 408 amino acids overlapping the P binding site in the same region of L. To identify amino acids important for binding P and L, site-directed mutagenesis of the L-408 protein was performed. Seven of twelve mutants in L-408 were unable to form a complex with measles P while the remainder did bind at least some P. In contrast, all of the mutants retained the ability to form the L-L complex, so different amino acids are involved in the L and P binding sites on L. Four of the 408 mutations defective in P binding were inserted into the full-length measles L protein and all retained L-L complex formation, but did not bind P. Full-length L mutants that did not bind P were also inactive in viral RNA synthesis, showing a direct correlation between P-L complex formation and activity.

Binding Sites↗
PubMed1995

Entry and release of measles virus are polarized in epithelial cells.

The initial site of virus replication during measles infection is in the epithelial cells of the respiratory tract. We have investigated measles virus infection of two types of polarized epithelial cells to determine if entry and/or release of the virus is confined to either the apical or the basolateral plasma membrane. The Caco-2 line of human intestinal epithelial cells and the polarized Vero C1008 monkey kidney cell line were grown on permeable supports and inoculated either through the apical or basolateral surfaces. Cells exposed to virus in the apical medium showed high levels of synthesis of virus-specific proteins, whereas no synthesis of viral proteins was detected in cells inoculated at the basolateral surface. Virus titers derived from apically infected cells were found to be about 1000-fold greater than titers derived from cells infected at the basolateral surface. Indirect immunofluorescence results also demonstrated that expression of measles viral antigens occurs at high levels only when input virions are inoculated at the apical surface. To investigate the localization of CD46 and moesin, which are receptors for measles virus, Caco-2 cells were incubated with monoclonal antibodies against CD46 or moesin followed by 125I-labeled anti-mouse Ig. The results indicate that CD46 is expressed preferentially on the apical membranes while moesin appears to be present at similar levels on both surfaces. Release of the virus was also examined and found to be polarized as well. Virus was released into the apical medium at up to 1000-fold higher titers than virus released into the basolateral medium. These results demonstrate that in two epithelial cell types measles virus preferentially enters and is released from epithelial cells in a polarized fashion through the apical plasma membrane.

Animals↗
PubMed1990

Effect of primary Epstein-Barr virus infection on human herpesvirus 6, cytomegalovirus, and measles virus immunoglobulin G titers.

Immunoglobulin G antibody titers to human herpesvirus 6 (HHV-6), measles virus, and cytomegalovirus (CMV) were examined in serum samples from 31 patients with Epstein-Barr virus (EBV)-induced infectious mononucleosis (IM). Sera were drawn sequentially from the same patients less than or equal to 7 days until 3 years after onset of IM. In seropositive patients, there was a significant decrease with time after IM of the immunoglobulin G titers to the three viruses in the majority of patients; HHV-6 IgG titers decreased in 80%, measles virus IgG titers decreased in 75%, and CMV IgG titers decreased in 67%. Four patients contracted CMV infection during the observation period after IM. In these, HHV-6 IgG titers increased, while EBV and measles virus IgG titers remained essentially stationary. Polyclonal B-cell stimulation during IM is suggested to augment antiviral titers in general, but the increases of HHV-6 IgG titers during EBV and CMV infections may also be due to selective stimulation of memory B cells by related antigens or to reactivation of HHV-6 during infection with these herpesviruses.

Adolescent↗
PubMedDate not supplied

Genetic characterization of wild-type measles viruses isolated during the 1998 measles epidemic in Argentina.

This study reports on genomic characterization of six measles virus (MV) isolates obtained from a measles epidemic in Argentina in 1998. Reverse transcription-polymerase chain reaction (RT-PCR) and nucleotide sequence analysis of the carboxyl-terminal region of the nucleoprotein (N) gene of these isolates classified all of them as wild type MV of D6 genotype. MVs of D6 genotype with identical nucleotide sequences in the region analyzed were also identified during the 1997 measles epidemic in Brazil and the 1999 measles outbreak in Uruguai. These results suggest that the MVs associated with the 1998 measles epidemic in Argentina might have originated from Brazil. As the D6 genotype is also widely distributed in Europe, it is possible that this genotype was brought to South America from Europe.

Adult↗
PubMed1986

Viruses disrupt functions of human lymphocytes. II. Measles virus suppresses antibody production by acting on B lymphocytes.

Measles virus infection is associated with suppression of immune functions both in vivo and in vitro. The virus infects T lymphocytes, B lymphocytes, and monocytes, but does not produce cytolysis. One consequence of infection in vitro is the failure of T and B lymphocyte mixtures to cooperate in secreting Ig in a PWM-driven system. Here we report that this defect in Ig secretion resides in the infected B lymphocyte, but not in the T lymphocyte or monocyte. Further, NK cells are not involved, since neither their depletion nor reconstitution abrogates suppression of B cell function. Proliferation of B cells in the early culture period is suppressed, suggesting that measles virus suppresses B cell development at the activation or proliferation stages, but does not affect terminal differentiation into Ig secreting cells.

Antibody Formation↗
PubMed2005

In vitro suppression of human immunodeficiency virus type 1 replication by measles virus.

During the acute phase of measles, human immunodeficiency virus type 1 (HIV-1)-infected children have a transient, but dramatic, decrease in plasma HIV-1 RNA levels (W. J. Moss, J. J. Ryon, M. Monze, F. Cutts, T. C. Quinn, and D. E. Griffin, J. Infect. Dis. 185:1035-1042, 2002). To determine the mechanism(s) by which coinfection with measles virus (MV) decreases HIV-1 replication, we established an in vitro culture system that reproduces this effect. The addition of MV to CCR5- or CXCR4-tropic HIV-1-infected human peripheral blood mononuclear cells (PBMCs) decreased HIV-1 p24 antigen production in a dose-dependent manner. This decrease occurred with the addition of MV before or after HIV-1. The inhibition of HIV-1 p24 antigen production was decreased when UV-inactivated MV or virus-free supernatant fluid from MV-infected PBMCs was used. Inhibition was not due to increased production of chemokines known to block coreceptor usage by HIV-1, a decrease in the percentage of CD4+ T cells, or a decrease in chemokine receptor expression by CD4+ T cells. Viability of PBMCs was decreased only 10 to 20% by MV coinfection; however, lymphocyte proliferation was decreased by 60 to 90% and correlated with decreased production of p24 antigen. These studies showed that an in vitro system of coinfected PBMCs could be used to dissect the mechanism(s) by which MV suppresses HIV-1 replication in coinfected children and suggest that inhibition of lymphocyte proliferation by MV may play a role in the suppression of HIV-1 p24 antigen production.

CD4 Antigens↗
PubMed1984

Purification, morphology and antigenic characterization of measles virus envelope components.

Measles virus haemagglutinin (H), fusion (F) and matrix (M) components were purified by affinity chromatography using monoclonal antibodies coupled to CNBr-activated Sepharose. H and M proteins were purified to homogeneity as determined by polyacrylamide gel electrophoresis by a single cycle of adsorption-desorption. The corresponding purification of the F protein required two cycles of adsorption-desorption. After the second adsorption an extra wash with 1 M-guanidine-HCl was employed to remove the contaminating cellular actin. Electron microscopic examination of the purified envelope proteins showed that, at pH 6.0, the H peplomers had a truncated conical shape (width 6.5 to 4 nm, length 16 nm), and the F peplomers had a club-like shape (dimensions of the oval head 6 X 9 nm, length 15 nm). Lengths of both peplomers were measured excluding their undiscernible hydrophobic part. The M component at pH 3.0 appeared as a rounded particle (diam. 8 nm, central accumulation of contrast 1.5 nm) suggested to include four to six M polypeptides. Rabbit hyperimmune sera were prepared against all three purified envelope components. These sera reacted only with the homologous antigen in radioimmunoprecipitation assays. Both antisera against the H and F components neutralized the virus and blocked virus-specific haemolysis, but only anti-H serum inhibited haemagglutination.

Animals↗
PubMed2005

Rescue and propagation of fully retargeted oncolytic measles viruses.

Live attenuated measles viruses of the Edmonston lineage (MV-Edm) have potent anti-tumor activity but are not entirely tumor-specific owing to widespread distribution of their native receptors, CD46 and SLAM. We have therefore developed a pseudoreceptor system that allows rescue and propagation of fully retargeted viruses displaying single-chain antibody fragments. Viruses retargeted to tumor-selective CD38, epidermal growth factor receptor (EGFR) or EGFR mutant vIII (EGFRvIII) efficiently entered cells through their respective targeted receptors in vitro and in vivo, but not through CD46 and SLAM. When administered intratumorally or intravenously to mice bearing human CD38 or EGFR-positive human tumor xenografts, the targeted viruses demonstrated specific receptor-mediated anti-tumor activity. These data provide an in vivo demonstration of antibody-directed tumor destruction by retargeted oncolytic viruses.

Animals↗
PubMed2005

Langerhans cells stimulated by mechanical stress are susceptible to measles virus infection.

OBJECTIVE: Measles virus (MV) first infects the human respiratory tract, but the initial target cells are unknown. We examined whether MV infects Langerhans cell-like dendritic cells (LCs) generated from CD14(+) monocytes in the presence of GM-CSF, IL-4, and TGF-beta1. METHODS: Cultured LCs were established as described recently [Biochem Biophys Res Commun 2003;306:674-679]. The expression of immunological markers was detected by FACScan. Infection with MV was assessed by syncytia formation, viral-specific fluorescence, and Western blotting. RESULTS: MV did not infect and replicate the freshly established, unstimulated LCs expressing CD1a, E-cadherin and Langerin but not CD83. Also, CD150, a receptor for MV was not expressed on the surface of the LCs. However, LCs stimulated by mechanical stress such as washing and centrifugation became susceptible to MV infection. CONCLUSION: A subset of mechanically stimulated LCs but not unstimulated immature ones became susceptible to MV. The actual role of Langerhans cells in local immunity seems to be to suppress unfavorable reactions initiated by virus intrusion.

Antigens, CD↗
PubMed1994

Characterization of a secreted form of measles virus haemagglutinin expressed from a vaccinia virus recombinant.

The measles virus (MV) haemagglutinin (HA) is a class 2 glycoprotein by means of which the virus particle attaches to the host cell receptor. We have previously expressed this glycoprotein as a vaccinia recombinant virus and have shown that the HA glycoprotein synthesized is indistinguishable from that coded by MV. In the present study, we report that in RK13 cells a soluble form (sHA) of the HA is secreted into the medium. We show by SDS-PAGE and sucrose density gradient centrifugation that the sHA is a dimer and is smaller than the cell-associated form. Using a variety of inhibitors the production of sHA was shown to be a late event, probably occurring at the membrane; only fully glycosylated molecules were found in sHA. Finally, we demonstrate that sHA retains its antigenicity with conformation-dependent MAbs and its receptor recognition function. We conclude that sHA is a valuable tool for use in studies of the structure and function of the MV HA glycoprotein.

Antibodies, Monoclonal↗
PubMed1999

Infection of chicken embryonic fibroblasts by measles virus: adaptation at the virus entry level.

Measles virus (MV) has a tropism restricted to humans and primates and uses the human CD46 molecule as a cellular receptor. MV has been adapted to grow in chicken embryonic fibroblasts (CEF) and gave rise to an attenuated live vaccine. Hallé and Schwarz MV strains were compared in their ability to infect both simian Vero cells and CEF. Whereas both strains infected Vero cells, only the CEF-adapted Schwarz strain was able to efficiently infect CEF. Since the expression of the human MV receptor CD46 rendered the chicken embryonic cell line TCF more permissive to the infection by the Hallé MV strain, the MV entry into CEF appeared to be a limiting step in the absence of prior MV adaptation. CEF lacked reactivity with anti-CD46 antibodies but were found to express another protein allowing MV binding as an alternative receptor to CD46.

Adaptation, Physiological↗