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PubMed2006

Cocirculation of measles virus genotype B2 and B3.1 in Central African Republic during the 2000 measles epidemic.

Many African countries have begun implementation of national programs to eliminate measles by the year 2015. However, measles continues to be endemic in Africa. This study describes the first molecular epidemiological study of measles virus circulating in Central African Republic. Two hundred and ten blood samples were tested for measles IgM. Sixty-seven urine samples were collected during measles outbreak in Bangui in 2000 and 2004 and used for genotyping studies. Two different methods were used to determine measles virus genotypes; the recently described real-time PCR-based method and the nucleotide sequencing and phylogenetic analysis methods. These tests revealed the cocirculation of two distinct viruses in Bangui. The proposed subgroup of the B3 genotype, B3.1 was found in 14 samples. This virus has been found in other neighboring countries. More surprising, genotype B2 was found in samples from four patients. The first measles genotype B2 viruses were isolated in Gabon in 1984, but have not been detected until recently when they were identified during a measles outbreak in 2003 in South Africa. This suggests that the circulation of measles genotype B2 has continued in Central Africa during the last 20 years. This study provides the baseline for genetic surveillance of measles virus in Central African Republic. Knowledge of currently circulating measles virus genotype in Central African Republic will help in monitoring the success of measles elimination program.

Base Sequence↗
PubMed1977

Measles virus meningoencephalitis. Immunofluorescence study of brains infected with virus mutants.

The localization of measles virus antigens in hamster brains inoculated with a temperature-sensitive mutant of measles virus r its revertant was studied by immunofluorescence. We found significantly less virus antigen in mutant-inoculated than in revertant-inoculated brains. In mutant-inoculated brains the virus antigens were very often found in the meninges. Possible mechanisms for the development of experimental hydrocephalus and meningoencephalitis are discussed.

Animals↗
PubMed1998

Modulation of immune system function by measles virus infection: role of soluble factor and direct infection.

Measles virus infection can result in a variety of immunologic defects. We have begun studies to determine the basis for the lack of immune responsiveness to antigen and mitogen following infection. Here we present data showing that Epstein-Barr virus-transformed B-cell lines infected with measles virus produce a soluble factor that can inhibit antigen-specific T-cell proliferation and inhibit the proliferation of uninfected B cells. The soluble factor was neither interleukin-10, transforming growth factor beta, nor alpha/beta interferon. B cells infected with measles virus or treated with the soluble factor were unable to present antigen to T cells in a manner that supported antigen-specific proliferation. This could represent one mechanism of how measles virus limits T-cell expansion. However, we found that once CD4(+) or CD8(+) T cells were activated, their cytolytic activity was intact whether infected with measles virus or treated with soluble factor. Thus, while slow to be generated these cytoxic cells could participate in viral clearance.

Antigen Presentation↗
PubMed1975

Replication and persistence of measles virus in defined subpopulations of human leukocytes.

Replication of Edmonston strain measles virus was studied in several human lymphoblast lines, as well as in defined subpopulations of circulating human leukocytes. It was found that measles virus can productively infect T cells, B cells, and monocytes from human blood. These conclusions were derived from infectious center studies on segregated cell populations, as well as from ultrastructural analyses on cells labeled with specific markers. In contrast, mature polymorphonuclear cells failed to synthesize measles virus nucleocapsids even after infection at a relatively high multiplicity of infection. Measles virus replicated more efficiently in lymphocytes stimulated with mitogens than in unstimulated cells. However, both phytohemagglutinin and pokeweed mitogen had a negligible stimulatory effect on viral synthesis in purified populations of monocytes. In all instances the efficiency of measles virus replication by monocytes was appreciably less than that of mitogenically stimulated lymphocytes or of continuously culture lymphoblasts. Under standard conditions of infection, all of the surveyed lymphoblast lines produced equivalent amounts of measles virus regardless of the major histocompatibility (HL-A) haplotype. Hence, no evidence was found that the HL-A3,7 haplotype conferred either an advantage or disadvantage with respect to measles virus synthesis in an immunologically neutral environment. A persistent infection with measles virus could be established in both T and B lymphoblasts. The release of infectious virus from such persistently infected cells was stable over a period of several weeks and was approximately 100-fold less than peak viral titers obtained in each respective line after acute infection.

B-Lymphocytes↗
PubMedDate not supplied

Measles virus was present in the inner cell of the acrosyringium in the skin rash.

A case of measles in a 26-year-old Japanese man is reported. A skin specimen taken on the third eruptive day from a maculopapular eruption on his chest was immunohistopathologically and electron microscopically examined using a rabbit polyclonal antibody against the nucleocapsid protein of the measles virus. The measles virus antigen was found in the inner cells of the acrosyringium and hair follicles. The measles virus nucleocapsid was electron microscopically identified in the nuclei of the inner cells of the acrosyringium. The findings suggest that the sweat from skin lesions might contain the measles virus.

Adult↗
PubMed2004

Effector CD8+T cells are suppressed by measles virus infection during delayed type hypersensitivity reaction.

Measles virus infection reduces or abolishes delayed type hypersensitivity reactions (DTH) in humans. We have previously shown that the primary 2,4-dinitrofluorobenzene (DNFB) response is temporarily suppressed by measles virus in cotton rats. Here, we demonstrate that also the secondary DNFB response (cutaneous hypersensitivity [CHS]) is suppressed in cotton rats by measles virus infection. As in mice, DNFB specific CD8 T cells are the predominant T cell response in cotton rats. After MV infection, CD8 T cells are reduced in their proliferative capacity whereas the CD4/CD8 ratio, the number and activation status of CD8 T cells is not affected. As a result of impaired proliferation of DNFB specific T cells the DTH response (measured as ear swelling) is reduced in measles virus infected cotton rats. At the same time as DNFB specific T cell responses are suppressed, spontaneous proliferation of lymphocytes as evidence for immune activation is found.

Animals↗
PubMed1999

Expression of interleukin-2 (IL-2) receptor alpha and CD45RO antigen on T-lymphocytes cultured with measles virus antigens, compared with humoral immunity in measles vaccinees.

In response to two types of measles virus (MV) antigens, a vaccine strain CAM and a wild strain isolated in 1994, the expression of IL-2 receptor alpha (CD25)(+)CD45RO(+)CD4(+) T-lymphocytes (T-cell activation) was analyzed by flow cytometry. In 75 healthy subjects with measles hemagglutination inhibition tests > or =1:16, the percentage of T-cell activation was significantly increased compared with that in seronegative individuals (p) < 0.05). Moreover, the T-cell expression was not significantly different among the vaccinated (n = 38), the naturally infected (n = 28) and the subclinically infected (exposed with wild type without history of measles infection and HI titers > or =1:16) (n = 10) groups. T-cell activation stimulated with MV antigens and HI antibody titers persisted for almost 30 years in the vaccinated group. These results suggest that cell-mediated immunity persists for long periods after vaccination and does not be influenced by antigenic drift.

Adolescent↗
PubMed1980

[Study of immunosuppressive effect of measles virus. In vitro effect of the leukocyte migration inhibition test (author's transl)].

The effects of the influence of the measles virus, further-attenuated measles virus, autoclaved measles virus, mumps virus and polio virus were investigated on the direct leukocyte migration inhibition test by agarose-droplet method using purified protein derivative as the antigen. It was found that the measles virus either inhibited the production of the leukocyte migration inhibition factor or inhibited the effect thereof. From this discovery, the mechanism of the suppression of delayed type hypersensitivity by measles virus was discussed.

Animals↗
PubMed1994

Measles virus induction of human endothelial cell tissue factor procoagulant activity in vitro.

Measles virus infection of microvascular endothelium in vivo and ensuing endothelial cell activation may be important in the pathogenesis of subsequent inflammation in target organs. This study investigated the capacity of measles virus to induce procoagulant activity, in vitro, in endothelial cells isolated from human umbilical cord veins. Endothelial cells were infected with a clinical isolate of measles virus propagated in Vero cells. Cells were also incubated with bacterial lipopolysaccharide (10 micrograms/ml), herpes simplex virus type 1, cytomegalovirus or culture medium alone as positive and negative controls, respectively. Endothelial cell procoagulant activity was measured in a one-stage clotting assay. Measles virus stimulated both a time and dose-dependent endothelial cell procoagulant response by the induction of tissue factor synthesis, confirmed by both immunocytochemistry and its dependence on factor VII for activity. This activity was reduced by u.v.-irradiation of the virus. Infected cells were analysed by double immunofluorescent staining for both tissue factor and measles virus N-protein, and examined using confocal scanning laser microscopy. Cells expressing tissue factor were also positive for the measles virus N-protein. Low levels of interleukin-1 were detected in some viral inocula derived from measles virus-infected Vero cells, however neutralising antibody to interleukin-1 failed to inhibit the endothelial cell procoagulant response to measles virus, whereas it significantly reduced procoagulant activity induced in endothelial cells by recombinant interleukin-1. The capacity of measles virus to induce endothelial tissue factor in vitro, may be relevant to the thrombotic vasculopathy associated with measles virus infection in vivo.

Animals↗
PubMed2002

Measles virus genome detected up to four months in a case of congenital measles.

UNLABELLED: To determine how long the measles virus genome was detected in a patient with congenital measles, the peripheral blood mononuclear cells were tested for 203 d. The measles virus genome was detected up to 140 d. CONCLUSION: The period for which the measles virus genome was detected in this patient with congenital measles was much longer than in normal children with measles.

Female↗
PubMed1986

Measles virus nucleic acid sequences in human brain.

We constructed a measles virus genomic recombinant DNA library, and used clones coding for portions of the viral P, M and H proteins to probe for measles virus nucleic acid sequences in post-mortem multiple sclerosis, SSPE and control brains. By dot blot hybridization, the probes detected measles virus nucleic acid sequences in as little as 3 nanograms of total RNA extracted from measles virus-infected cells and also in highly diluted RNA extracted from SSPE brain, but did not detect measles virus sequences in RNA extracted from 11 multiple sclerosis or 8 control brains, even at a 1 000-fold higher concentration of RNA. By in situ hybridization, these probes detected measles virus nucleic acid sequences in virtually every cell and the surrounding neuropile of SSPE brain, but again did not detect such sequences in multiple sclerosis or control brains. Our findings using these highly specific probes confirm that measles virus is found in SSPE brains and indicate that measles virus genome is unlikely to be present in multiple sclerosis or normal brains.

Base Sequence↗
PubMed1997

Isolation of a measles virus variant: protection of newborn mice from measles encephalitis by 24 h prior intracerebral inoculation with the variant.

A small plaque mutant with reduced neurovirulence in newborn mice was obtained from Edmonston strain measles virus after propagation for 5 months in NIH3T3 cells. It retained the antigenicity of the parental virus and tended to induce higher neutralizing antibody titers in the adult BALB/c mice. The intracerebral (but not intraperitoneal) inoculation of the live mutant virus one day before prevented the newborn BALB/c mice from encephalitis caused by the intracerebral challenge with the parental strain at a dose of 10-20 LD50. The intracerebral inoculation with the mutant virus whose replication capacity was inactivated by UV-irradiation was ineffective. The protection was not attributed to interferons nor to viral interference. The mechanism remains unknown.

3T3 Cells↗
PubMed1979

Role of virus variants and cells in maintenance of persistent infection by measles virus.

Hamster embryo fibroblasts persistently infected with a derivative of the Schwarz vaccine strain of measles virus spontaneously released virus particles with an average buoyant density considerably lower than that of the parental virus. The released virus contained all of the measles virus structural proteins and interfered with replication of standard virus. All of the virus structural proteins were associated with a membrane-free cytoplasmic extract from the persistently infected cells. Membrane-free cytoplasmic extracts prepared from Vero cells lytically infected with Schwarz strain measles contained little or no virus envelope structural protein. Maintenance of persistent infection may involve both the presence of virus variants and a defect in the ability of the infected cell to replicate the virus efficiently.

Animals↗
PubMed1976

Cytolytic, complement-dependent antibodies to measles virus in rhesus monkeys after administration of live or killed virus.

Infection of rhesus monkeys with measles virus induced specific complement-dependent cytolytic antibodies during the early phase of acute infection. The development of maximal levels of the complement-dependent cytolytic antibodies appears to be dependent on the respiratory rather than the parenteral route of infection and on the use of live rather than killed measles virus. These levels of cytolytic antibodies seem to be independent of levels of simultaneously developing neutralizing and hemagglutinating antibodies. It is proposed that complement-dependent cytolytic antibodies play an important role in the elimination of acute measles virus in vivo by lysing the foci of infected cells and by blocking the spread of virus by cell fusion.

Animals↗
PubMed1999

Measles virus infection induces terminal differentiation of human thymic epithelial cells.

Measles virus infection induces a profound immunosuppression that may lead to serious secondary infections and mortality. In this report, we show that the human cortical thymic epithelial cell line is highly susceptible to measles virus infection in vitro, resulting in infectious viral particle production and syncytium formation. Measles virus inhibits thymic epithelial cell growth and induces an arrest in the G0/G1 phases of the cell cycle. Moreover, we show that measles virus induces a progressive thymic epithelial cell differentiation process: attached measles virus-infected epithelial cells correspond to an intermediate state of differentiation while floating cells, recovered from cell culture supernatants, are fully differentiated. Measles virus-induced thymic epithelial cell differentiation is characterized by morphological and phenotypic changes. Measles virus-infected attached cells present fusiform and stellate shapes followed by a loss of cell-cell contacts and a shift from low- to high-molecular-weight keratin expression. Measles virus infection induces thymic epithelial cell apoptosis in terminally differentiated cells, revealed by the condensation and degradation of DNA in measles virus-infected floating thymic epithelial cells. Because thymic epithelial cells are required for the generation of immunocompetent T lymphocytes, our results suggest that measles virus-induced terminal differentiation of thymic epithelial cells may contribute to immunosuppression, particularly in children, in whom the thymic microenvironment is of critical importance for the development and maturation of a functional immune system.

Apoptosis↗
PubMed1984

Low antibody response in infants with measles and children with subclinical measles virus infection.

During a measles epidemic (December 1979-March 1980) in two adjacent villages in Tamil Nadu, 78 of 143 under-fives were affected, eight of whom died, giving an attack rate of 54% and case-fatality rate of 10%. Seven months later 72 children (41 with measles, seven with history of measles in prior epidemics and 24 with no history of measles) were bled to measure measles virus haemagglutination-inhibition antibody. Of the 48 with measles history, 46 had measurable antibody. Surprisingly, of the 24 without a history, 16 had measurable antibody indicating the frequency of subclinical measles during epidemics. The geometric mean antibody titre was lower in infants with measles than in older children (P less than 0.05). The mean titre was lower in those with subclinical measles than in those with clinical measles (P less than 0.01).

Age Factors↗
PubMed2001

[Effects of attenuated measles virus on hepatitis B virus in vivo and in vitro].

OBJECTIVE: To observe the effects of attenuated measles virus on hepatitis B virus replication inside and outside the body. METHODS: Patients with chronic hepatitis B virus replication were chosen, and attenuated measles viruses were inoculated in them and observed twice every week for a total of 48 weeks. The changes of CD4+, CD8+, IFN-gamma, IL-2, HBeAg and HBV DAN were observed. Also the changes of the HBVM were observed when adding the measles virus in suspension of the 2.2.15 cells. RESULTS: The average ratio of CD4+ and CD8+ before the treatment was 1.05 +/- 0.19 and it rose to 1.47 +/- 0.18 after follow up for 48 weeks. Then, compared with the ratio before the treatment, the difference was significant(t = 5.36, P < 0.01). After inoculating the measles virus for two weeks, IFN-gamma and IL-2 increased. Although the total average ratio had not great difference, IL-2 level of 26.3% of the cases elevated 5 times higher in the second week, as compared with the control group, there was a great difference (chi 2 = 12.07, P < 0.005). The results of the examination of the HBeAg before treatment was 317, 35 +/- 151.75, but became 139.17 +/- 166.66 after observing for 48 weeks(t = 2.16, P < 0.05). The positive ratio of HBV DNA before the treatment was 100% and become 63.16% after treatment. Thus the ratio difference is significant(chi 2 = 10.08, P < 0.005). However, no such ratio difference was found in the control group. When adding the attenuated measles virus in suspension of 2.2.15 cell, the HBsAg and HBeAg decreased. CONCLUSION: When the measles virus and hepatitis B virus infect the cases in an overlapping way, the latter may be interfered by change of the cell immunity status of the body of the former, and measles virus may have direct interference effects on hepatitis B virus.

Adult↗