Rubella virus: The type (and only) species of RUBIVIRUS causing acute infection in humans, primarily children and young adults. Humans are the only natural host. A live, attenuated vaccine is available for prophylaxis.Rubella: An acute infectious disease caused by the RUBELLA VIRUS. The virus enters the respiratory tract via airborne droplet and spreads to the LYMPHATIC SYSTEM.Rubella Vaccine: A live attenuated virus vaccine of duck embryo or human diploid cell tissue culture origin, used for routine immunization of children and for immunization of nonpregnant adolescent and adult females of childbearing age who are unimmunized and do not have serum antibodies to rubella. Children are usually immunized with measles-mumps-rubella combination vaccine. (Dorland, 28th ed)Rubella Syndrome, Congenital: Transplacental infection of the fetus with rubella usually in the first trimester of pregnancy, as a consequence of maternal infection, resulting in various developmental abnormalities in the newborn infant. They include cardiac and ocular lesions, deafness, microcephaly, mental retardation, and generalized growth retardation. (From Dorland, 27th ed)Hemagglutination Inhibition Tests: Serologic tests in which a known quantity of antigen is added to the serum prior to the addition of a red cell suspension. Reaction result is expressed as the smallest amount of antigen which causes complete inhibition of hemagglutination.Antibodies, Viral: Immunoglobulins produced in response to VIRAL ANTIGENS.Vero Cells: A CELL LINE derived from the kidney of the African green (vervet) monkey, (CERCOPITHECUS AETHIOPS) used primarily in virus replication studies and plaque assays.Virus Cultivation: Process of growing viruses in live animals, plants, or cultured cells.Measles-Mumps-Rubella Vaccine: A combined vaccine used to prevent MEASLES; MUMPS; and RUBELLA.Mumps: An acute infectious disease caused by RUBULAVIRUS, spread by direct contact, airborne droplet nuclei, fomites contaminated by infectious saliva, and perhaps urine, and usually seen in children under the age of 15, although adults may also be affected. (From Dorland, 28th ed)Measles virus: The type species of MORBILLIVIRUS and the cause of the highly infectious human disease MEASLES, which affects mostly children.RNA Viruses: Viruses whose genetic material is RNA.Cercopithecus aethiops: A species of CERCOPITHECUS containing three subspecies: C. tantalus, C. pygerythrus, and C. sabeus. They are found in the forests and savannah of Africa. The African green monkey (C. pygerythrus) is the natural host of SIMIAN IMMUNODEFICIENCY VIRUS and is used in AIDS research.Virus Replication: The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.Measles: A highly contagious infectious disease caused by MORBILLIVIRUS, common among children but also seen in the nonimmune of any age, in which the virus enters the respiratory tract via droplet nuclei and multiplies in the epithelial cells, spreading throughout the MONONUCLEAR PHAGOCYTE SYSTEM.Immunoglobulin M: A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.Vaccinia virus: The type species of ORTHOPOXVIRUS, related to COWPOX VIRUS, but whose true origin is unknown. It has been used as a live vaccine against SMALLPOX. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of VACCINIA VIRUS.Virus Assembly: The assembly of VIRAL STRUCTURAL PROTEINS and nucleic acid (VIRAL DNA or VIRAL RNA) to form a VIRUS PARTICLE.RNA, Viral: Ribonucleic acid that makes up the genetic material of viruses.Mumps virus: The type species of RUBULAVIRUS that causes an acute infectious disease in humans, affecting mainly children. Transmission occurs by droplet infection.Antigens, Viral: Substances elaborated by viruses that have antigenic activity.Sindbis Virus: The type species of ALPHAVIRUS normally transmitted to birds by CULEX mosquitoes in Egypt, South Africa, India, Malaya, the Philippines, and Australia. It may be associated with fever in humans. Serotypes (differing by less than 17% in nucleotide sequence) include Babanki, Kyzylagach, and Ockelbo viruses.Immunoglobulin G: The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.Pregnancy Complications, Infectious: The co-occurrence of pregnancy and an INFECTION. The infection may precede or follow FERTILIZATION.Receptors, Virus: Specific molecular components of the cell capable of recognizing and interacting with a virus, and which, after binding it, are capable of generating some signal that initiates the chain of events leading to the biological response.Virus Diseases: A general term for diseases produced by viruses.Virus Shedding: The expelling of virus particles from the body. Important routes include the respiratory tract, genital tract, and intestinal tract. Virus shedding is an important means of vertical transmission (INFECTIOUS DISEASE TRANSMISSION, VERTICAL).Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis.Hemagglutination, Viral: Agglutination of ERYTHROCYTES by a virus.Simian virus 40: A species of POLYOMAVIRUS originally isolated from Rhesus monkey kidney tissue. It produces malignancy in human and newborn hamster kidney cell cultures.Haplorhini: A suborder of PRIMATES consisting of six families: CEBIDAE (some New World monkeys), ATELIDAE (some New World monkeys), CERCOPITHECIDAE (Old World monkeys), HYLOBATIDAE (gibbons and siamangs), CALLITRICHINAE (marmosets and tamarins), and HOMINIDAE (humans and great apes).Mumps Vaccine: Vaccines used to prevent infection by MUMPS VIRUS. Best known is the live attenuated virus vaccine of chick embryo origin, used for routine immunization of children and for immunization of adolescents and adults who have not had mumps or been immunized with live mumps vaccine. Children are usually immunized with measles-mumps-rubella combination vaccine.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Plant Viruses: Viruses parasitic on plants higher than bacteria.Viral Proteins: Proteins found in any species of virus.Cytopathogenic Effect, Viral: Visible morphologic changes in cells infected with viruses. It includes shutdown of cellular RNA and protein synthesis, cell fusion, release of lysosomal enzymes, changes in cell membrane permeability, diffuse changes in intracellular structures, presence of viral inclusion bodies, and chromosomal aberrations. It excludes malignant transformation, which is CELL TRANSFORMATION, VIRAL. Viral cytopathogenic effects provide a valuable method for identifying and classifying the infecting viruses.DNA Viruses: Viruses whose nucleic acid is DNA.Viral Envelope Proteins: Layers of protein which surround the capsid in animal viruses with tubular nucleocapsids. The envelope consists of an inner layer of lipids and virus specified proteins also called membrane or matrix proteins. The outer layer consists of one or more types of morphological subunits called peplomers which project from the viral envelope; this layer always consists of glycoproteins.Kaolin: The most common mineral of a group of hydrated aluminum silicates, approximately H2Al2Si2O8-H2O. It is prepared for pharmaceutical and medicinal purposes by levigating with water to remove sand, etc. (From Merck Index, 11th ed) The name is derived from Kao-ling (Chinese: "high ridge"), the original site. (From Grant & Hackh's Chemical Dictionary, 5th ed)Defective Viruses: Viruses which lack a complete genome so that they cannot completely replicate or cannot form a protein coat. Some are host-dependent defectives, meaning they can replicate only in cell systems which provide the particular genetic function which they lack. Others, called SATELLITE VIRUSES, are able to replicate only when their genetic defect is complemented by a helper virus.Genes, Viral: The functional hereditary units of VIRUSES.Influenza A Virus, H1N1 Subtype: A subtype of INFLUENZA A VIRUS with the surface proteins hemagglutinin 1 and neuraminidase 1. The H1N1 subtype was responsible for the Spanish flu pandemic of 1918.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Neutralization Tests: The measurement of infection-blocking titer of ANTISERA by testing a series of dilutions for a given virus-antiserum interaction end-point, which is generally the dilution at which tissue cultures inoculated with the serum-virus mixtures demonstrate cytopathology (CPE) or the dilution at which 50% of test animals injected with serum-virus mixtures show infectivity (ID50) or die (LD50).Viral Structural Proteins: Viral proteins that are components of the mature assembled VIRUS PARTICLES. They may include nucleocapsid core proteins (gag proteins), enzymes packaged within the virus particle (pol proteins), and membrane components (env proteins). These do not include the proteins encoded in the VIRAL GENOME that are produced in infected cells but which are not packaged in the mature virus particle,i.e. the so called non-structural proteins (VIRAL NONSTRUCTURAL PROTEINS).Convalescence: The period of recovery following an illness.Seroepidemiologic Studies: EPIDEMIOLOGIC STUDIES based on the detection through serological testing of characteristic change in the serum level of specific ANTIBODIES. Latent subclinical infections and carrier states can thus be detected in addition to clinically overt cases.Rabies virus: The type species of LYSSAVIRUS causing rabies in humans and other animals. Transmission is mostly by animal bites through saliva. The virus is neurotropic multiplying in neurons and myotubes of vertebrates.Arboviruses: Arthropod-borne viruses. A non-taxonomic designation for viruses that can replicate in both vertebrate hosts and arthropod vectors. Included are some members of the following families: ARENAVIRIDAE; BUNYAVIRIDAE; REOVIRIDAE; TOGAVIRIDAE; and FLAVIVIRIDAE. (From Dictionary of Microbiology and Molecular Biology, 2nd ed)Influenza A Virus, H5N1 Subtype: A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 5 and neuraminidase 1. The H5N1 subtype, frequently referred to as the bird flu virus, is endemic in wild birds and very contagious among both domestic (POULTRY) and wild birds. It does not usually infect humans, but some cases have been reported.Cricetinae: A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.Viral Interference: A phenomenon in which infection by a first virus results in resistance of cells or tissues to infection by a second, unrelated virus.Pregnancy: The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.

Removal of non-specific serum inhibitors of haemagglutination of rubella virus by treatment with dodecylamine-gel. (1/550)

The suitability of using dodecylamine-gel for removing the serum non-antibody-like inhibitors of haemagglutination by rubella was studied. Compared with kaolin and MnCl2/heparin treatment this new procedure appears to have a higher specificity since it removes the non-antibody-like inhibitors from serum without affecting the immunoglobulin level significantly. The potential application of this procedure in routine serological analysis for rubella virus infection is discussed.  (+info)

Rubella virus-induced apoptosis varies among cell lines and is modulated by Bcl-XL and caspase inhibitors. (2/550)

Rubella virus (RV) causes multisystem birth defects in the fetuses of infected women. To investigate the cellular basis of this pathology, we examined the cytopathic effect of RV in three permissive cell lines: Vero 76, RK13, and BHK21. Electron microscopy and the TUNEL assay showed that the cytopathic effect resulted from RV-induced programmed cell death (apoptosis) in all three cell lines, but the extent of apoptosis varied among these cells. At 48 h postinfection, the RK13 cell line showed the greatest number of apoptotic cells, the Vero 76 cell line was approximately 3-fold less, and BHK21 had very few. An increased multiplicity of infection and longer time postinfection were required for the BHK21 cell line to reach the level of apoptotic cells in Vero 76 at 48 h. Purified RV induced apoptosis in a dose-dependent fashion, but not UV-inactivated RV or virus-depleted culture supernatant. Specific inhibitors of the apoptosis-specific proteases caspases reduced RV-induced apoptosis and led to higher levels of RV components in infected cells. To address the role of regulatory proteins in RV-induced apoptosis, the antiapoptotic gene Bcl-2 or Bcl-XL was transfected into RK13 cells. Although a high level of Bcl-2 family proteins was expressed, no protection was observed from apoptosis induced by RV, Sindbis virus, or staurosporine in RK13 cells. In BHK21 cells, however, increased expression of Bcl-XL protected cells from apoptosis. The observed variability in apoptotic response to RV of these cell lines demonstrates that programmed cell death is dependent on the unique properties of each cell and may be indicative of how selective organ damage occurs in a congenital rubella syndrome fetus.  (+info)

Mutations in the retinoblastoma protein-binding LXCXE motif of rubella virus putative replicase affect virus replication. (3/550)

The rubella virus (RV)-encoded protein NSP90, which contains the retinoblastoma protein (Rb)-binding motif LXCXE, interacts with Rb and RV replication is reduced in cells lacking Rb. Whether the LXCXE motif of RV NSP90 itself is essential for Rb binding and virus replication is not known. Therefore, in the present study, the functional role of this motif was investigated by site-directed mutagenesis in a plasmid from which infectious RV RNA can be produced. Three critical mutations in the motif, two substitutions at the conserved cysteine residue (C --> G and C --> R) and a deletion of the entire motif, were created. A cell-free translated NSP90 C terminus polypeptide containing the deletion did not bind to Rb and a polypeptide carrying the C --> R substitution had barely detectable binding affinity for Rb. Rb binding by the C --> G mutant was reduced significantly compared to that of wild-type protein. Correlating with the binding results, mutant viruses containing the LXRXE and LXGXE motifs had a reduction in replication to < 0.5% and 47% of the wild-type, respectively, while deletion of the motif was found to be lethal. By the first serial passage, replication of the LXRXE-carrying virus had increased from < 0.5% to 2% of the wild-type. Sequencing of the genome of this virus revealed a nucleotide change that altered the motif from LXRXE to LXSXE, which is a known Rb-binding motif in two protein phosphatase subunits. Thus, our results clearly demonstrate that the LXCXE motif is required for efficient RV replication.  (+info)

Mutagenic analysis of the 3' cis-acting elements of the rubella virus genome. (4/550)

Thermodynamically predicted secondary structure analysis of the 3'-terminal 305 nucleotides (nt) of the rubella virus (RUB) genome, a region conserved in all RUB defective interfering RNAs, revealed four stem-loop (SL) structures; SL1 and SL2 are both located in the E1 coding region, while SL3 and SL4 are within the 59-nt 3' untranslated region (UTR) preceding the poly(A) tract. SL2 is a structure shown to interact with human calreticulin (CAL), an autoantigen potentially involved in RUB RNA replication and pathogenesis. RNase mapping indicated that SL2 and SL3 are in equilibrium between two conformations, in the second of which the previously proposed CAL binding site in SL2, a U-U bulge, is not formed. Site-directed mutagenesis of the 3' UTR with a RUB infectious clone, Robo302, revealed that most of the 3' UTR is required for viral viability except for the 3'-terminal 5 nt and the poly(A) tract, although poly(A) was rapidly regenerated during subsequent replication. Maintenance of the overall SL3 structure, the 11-nt single-stranded sequence between SL3 and SL4, and the sequences forming SL4 were all important for viral viability. Studies on the interaction between host factors and the 3' UTR showed the formation of three RNA-protein complexes by gel mobility shift assay, and UV-induced cross-linking detected six host protein species, with molecular masses of 120, 80, 66, 55, 48, and 36 kDa, interacting with the 3' UTR. Site-directed mutagenesis of SL2 by nucleotide substitutions showed that maintenance of SL2 stem rather than the U-U bulge was critical in CAL binding since mutants having the U-U bulge base paired had a similar binding activity for CAL as the native structure whereas mutants having the SL2 stem destabilized had much lower binding activity. However, all of these mutations gave rise to viable viruses when introduced into Robo302, indicating that binding of CAL to SL2 is independent of viral viability.  (+info)

A modified rubella HI test using prestandardized reagents. (5/550)

A modified haemagglutination inhibition test for rubella antibodies using prestandardized freeze-dried reagents was compared to a "standard" method. Tests of 707 serum samples showed that the modified test was sensitive and reliable by both macrotitration and microtitration techniques. The minor disadvantages of some reduction in antibody level when rubella sera were tested within one week of the rash and of spontaneous sheep erythrocyte agglutination in 0-7% of sera were out-weighed by the increased speed of the new test and the fact that it was carried out at room temperature.  (+info)

Role of rubella virus glycoprotein domains in assembly of virus-like particles. (6/550)

Rubella virus is a small enveloped positive-strand RNA virus that assembles on intracellular membranes in a variety of cell types. The virus structural proteins contain all of the information necessary to mediate the assembly of virus-like particles in the Golgi complex. We have recently identified intracellular retention signals within the two viral envelope glycoproteins. E2 contains a Golgi retention signal in its transmembrane domain, whereas a signal for retention in the endoplasmic reticulum has been localized to the transmembrane and cytoplasmic domains of E1 (T. C. Hobman, L. Woodward, and M. G. Farquhar, Mol. Biol. Cell 6:7-20, 1995; T. C. Hobman, H. F. Lemon, and K. Jewell, J. Virol. 71:7670-7680, 1997). In the present study, we have analyzed the role of these retention signals in the assembly of rubella virus-like particles. Deletion or replacement of these domains with analogous regions from other type I membrane glycoproteins resulted in failure of rubella virus-like particles to be secreted from transfected cells. The E1 transmembrane and cytoplasmic domains were not required for targeting of the structural proteins to the Golgi complex and, surprisingly, assembly and budding of virus particles into the lumen of this organelle; however, the resultant particles were not secreted. In contrast, replacement or alteration of the E2 transmembrane or cytoplasmic domain, respectively, abrogated the targeting of the structural proteins to the budding site, and consequently, no virion formation was observed. These results indicate that the transmembrane and cytoplasmic domains of E2 and E1 are required for early and late steps respectively in the viral assembly pathway and that rubella virus morphogenesis is very different from that of the structurally similar alphaviruses.  (+info)

Mutational analysis, using a full-length rubella virus cDNA clone, of rubella virus E1 transmembrane and cytoplasmic domains required for virus release. (7/550)

We report on the construction of a full-length cDNA clone, pBRM33, derived from wild-type rubella virus M33 strain. The RNA transcripts synthesized in vitro from pBRM33 are highly infectious, and the viruses produced retain the phenotypic characteristics of the parental M33 virus in growth rate and plaque size. This cDNA clone was used to study the role of E1 transmembrane and cytoplasmic domains in virus assembly by site-directed mutagenesis. Three different alanine substitutions were introduced in the transmembrane domain of E1. These included substitution of leucine 464, cysteine 466, cysteine 467, and both cysteines 466 and 467 to alanine. In the E1 cytoplasmic domain, cysteine 470 and leucine 471 were altered to alanine. We found that these mutations did not significantly affect viral RNA replication, viral structural protein synthesis and transport, or E2/E1 heterodimer formation. Except for the substitution of cysteine 470, these mutations did, however, lead to a reduction in virus release. Substitution of cysteine 467 in the transmembrane region and of leucine 471 in the cytoplasmic domain dramatically reduced virus yield, resulting in the production of only 1 and 10% of the parental virus yield, respectively, in a parallel infection. These data show that E1 transmembrane and cytoplasmic domains play an important role in late stages of virus assembly, possibly during virus budding, consistent with earlier studies indicating that the E1 cytoplasmic domain may interact with nucleocapsids and that this interaction drives virus budding.  (+info)

Involvement of a p53-dependent pathway in rubella virus-induced apoptosis. (8/550)

In light of the important role of apoptotic cell death in the pathogenesis of several viral infections, we asked whether the cytopathogenicity evoked by rubella virus (RV) might also involve apoptotic mechanisms. The To-336 strain of RV induced apoptosis in Vero and RK-13 cells, but not in fibroblast cell lines. UV-inactivated RV virions did not elicit the apoptotic response, indicating that productive infection is required for the induction of cell death. Both p53 and p21 protein levels were highly elevated in RV-infected Vero cells. The level of p21 mRNA was increased, while expression of the p53 gene was unaffected by RV infection. A dominant-negative p53 mutant (p53(W248)) conferred partial protection from RV-induced apoptosis. These data implicate a p53-dependent apoptotic pathway in the cytopathogenicity of RV, thereby suggesting a mechanism by which RV exerts its teratogenic effects.  (+info)

  • Frey, T. K. 2003-01-02 00:00:00 Two genotypes of Rubella virus have been described that differ by 8-9% at the nucleotide level in the E1 glycoprotein gene. (deepdyve.com)
  • Carmo Sampaio Tavares Timenetsky, Maria 2014-06-01 00:00:00 The aim of the present study was to identify the rubella virus (RV) and enterovirus (EV) genotypes detected during the Epidemiological Surveillance on Exanthematic Febrile Diseases (VIGIFEX) study and to perform phylogenetic analysis. (deepdyve.com)
  • measles virus (mv) was classified in 24 genotypes that show a distinct geographic distribution. (liverpool.ac.uk)
  • Experts with the CDC and other health organizations caution that the virus could be reintroduced from other parts of the world, making immunization and public awareness continuing priorities. (edweek.org)
  • The announcement by the CDC is a caution that we have to keep immunization up, because if people aren't immunized [against rubella], it could spread," said Dr. Robert Baltimore, a professor of pediatrics at Yale University and a member of the American Academy of Pediatrics' committee on infectious diseases. (edweek.org)
  • The rubella virus, which causes a relatively mild respiratory disease in schoolchildren but can lead to serious birth defects in unborn children, is no longer a significant public-health threat in the United States, the federal Centers for Disease Control and Prevention announced last week. (edweek.org)
  • Norman Gregg , an ophthalmologist who linked rubella to birth defects, was an early advocate of the idea that infected pregnant women should have access to abortion. (nationalgeographic.com)
  • The United States suffered an outbreak of rubella in 1958, but it wasn't until after the thalidomide disaster in the early 1960s-when a drug given to pregnant women caused severe birth defects-that Americans really began to fear the effects of rubella. (nationalgeographic.com)
  • 1 Current address: Respiratory and Enteric Viruses Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA. (cdc.gov)
  • Rubella virus is the only member of the genus Rubivirus and belongs to the family of Togaviridae, whose members commonly have a genome of single-stranded RNA of positive polarity which is enclosed by an icosahedral capsid. (wikipedia.org)
  • Homologous sequences are present in the rubella genome. (wikipedia.org)
  • In the rubella genome these occur in the opposite orientation to that found in the alphaviruses indicating that a genome rearrangement has occurred. (wikipedia.org)
  • If you have rubella, you are most likely to spread it a few days before the rash starts until 5 to 7 days after the rash first appears. (wellspan.org)
  • If you or your child has rubella, don't go to work, school, or day care for 7 days after the rash first appears. (wellspan.org)
  • Group: ssRNA(+) Order: Unassigned Family: Togaviridae Genus: Rubivirus Rubella virus The spherical virus particles (virions) of Togaviridae have a diameter of 50 to 70 nm and are covered by a lipid membrane (viral envelope), derived from the host cell membrane. (wikipedia.org)
  • Rubella virus is an enveloped positive-strand RNA virus of the family TOGAVIRIDAE: Virions are composed of three structural proteins: a capsid and two membrane-spanning glycoproteins, E2 and E1. (acris-antibodies.com)
  • The genomes of these viruses all contained 9762 nts and the lengths of the three untranslated regions (UTRs) and two open reading frames (ORF's) were identical. (deepdyve.com)
  • From the ER the heterodimeric E1·E2-complex reaches the Golgi apparatus, where the budding of new virions occurs (unlike alpha viruses, where budding occurs at the plasma membrane. (wikipedia.org)