Antibodies to reoviruses, parainfluenza 3 virus, encephalomyocarditis virus and infectious bovine rhinotracheitis virus in porcine serums.
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Animals↗
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Analysis of nearest neighbour base frequencies in the RNA of a mammalian virus: encephalomyocarditis virus.
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Adenine↗
Photoinactivation of the encephalomyocarditis virus.
Encephalomyocarditis virus was photoinactivated by a dilution of 1:30,000 neutral red and 70 minutes exposure to light. A dye inactivation of the EMC virus is possible without destruction of its antigenicity. The EMC virus vaccine induced a good immunity response in mice; we did not find any infectious virus.
Animals↗
Polyamines in encephalomyocarditis virus.
Encephalomyocarditis virus contains approximately 200 molecules of putrescine, 100 molecules of spermidine, and 40 molecules of spermine which could neutralize 11% of the viral genome. The same polyamines are present in different proportions in the Krebs ascites tumor cell in which the virus was grown.
Cadaverine↗
Fatal disease of swine due to encephalomyocarditis virus.
Encephalomyocarditis virus was isolated from the organs of swine dying during an outbreak of an acutely fatal disease occurring on a farm in Panama. The outstanding lesion was severe myocarditis. Pigs inoculated with the viral isolate developed a systemic infection with myocarditis.
Animals↗
Outbreaks in Quebec pig farms of respiratory and reproductive problems associated with encephalomyocarditis virus.
Encephalomyocarditis virus (EMCV) was isolated from tissues of aborted fetuses and weaned and suckling piglets from 4 different pig farms in Quebec. The farms were experiencing reproductive failure in sows of different parities concomitant to respiratory problems in suckling and postweaning piglets. At necropsy, gross lesions were confined to the lung and consisted of pulmonary congestion and edema of various degrees. Lesions of multifocal interstitial to proliferative pneumonia were found in the lungs of these piglets. Bacteriologic examination of various tissues from necropsied pigs yielded no pathogens in most cases. No significant antibody titers against 3 swine viruses (transmissible gastroenteritis virus, porcine parvovirus, and swine influenza virus) and two bovine viruses (bovine viral diarrhea and infectious bovine rhinotracheitis viruses) were detected in the sera of convalescent pigs. The Quebec EMCV isolates were antigenically related to the reference ATCC-VR129 strain of EMCV, as demonstrated by indirect immunofluorescence, serum neutralization (SN), and Western immunoblotting. However, one of the Quebec isolates could be distinguish by SN. EMCV-specific SN antibody titers up to 1:12,800 were detected in thoracic and ascitis fluids of aborted fetuses and in sera of convalescent pigs. A possible pneumotropic EMCV variant in swine may exist.
Abortion, Veterinary↗
Defective interfering particles of encephalomyocarditis virus.
Encephalomyocarditis (EMC) virus and five temperature-sensitive mutants of EMC virus were serially passed numerous times in HeLa, L929 and BHK-21 cells. Equilibrium centrifugation in CsCl density gradients of virus and electrophoresis of virus RNA from many of the high number passages indicated the presence of standard EMC virus and particles containing RNA of lower molecular weight. Three virus isolates with high passage number were able to interfere with the replication of the standard virions in mixed infections. We believe our results show the generation of defective interfering particles of EMC virus.
Animals↗
Chloroquine enhances replication of Semliki Forest virus and encephalomyocarditis virus in mice.
Chloroquine (CHL) has been suggested to play an important role in the development of Burkitt's lymphoma by enhancing Epstein-Barr virus expression. Herpes zoster virus incidence is markedly increased following malaria infection in children being treated with CHL. Recently, CHL has also been shown to dramatically increase the transactivation of Tat protein purified from human immunodeficiency virus. These previous studies indirectly suggest that CHL may be involved in the enhancement of virus replication. This study demonstrates for the first time that CHL indeed enhances Semliki Forest virus and encephalomyocarditis virus replication in mice. These results raise the possible connection between the increased spread of AIDS in endemic malaria areas and the wide use of CHL in those areas for the chemotherapy of malaria.
Animals↗
Human interferon-alpha-and-gamma-mediated inhibition of retrovirus production in the absence of an inhibitory effect on vesicular stomatitis virus and encephalomyocarditis virus replication in RD-114 cells.
RD-114 line is a human sarcoma cell line chronically infected with RD-114 retrovirus. Treatment of these cells with increasing doses of human interferon-alpha or -gamma resulted in increasing inhibition of RD-114 virus production. Surprisingly, the replication of vesicular stomatitis virus and encephalomyocarditis virus, in these cells and in the parental RD cells which are not infected with the retrovirus, was insensitive to interferon treatment. Unlike reported differences in other properties of interferon-alpha and interferon-gamma, there were no differences in their antiretroviral properties such as dose response, kinetics of establishment of the antiretroviral state, and kinetics of its dissipation upon removal of interferon.
Dose-Response Relationship, Drug↗
Interferon-induced guanylate binding protein-1 (GBP-1) mediates an antiviral effect against vesicular stomatitis virus and encephalomyocarditis virus.
A cDNA encoding the human guanylate binding protein-1 (hGBP-1) was expressed in HeLa cells using a constitutive expression vector. Stably transfected clones expressing hGBP-1 exhibited resistance to the cytopathic effect mediated by both vesicular stomatitis virus (VSV) and encephalomyocarditis virus (EMCV) and produced less viral progeny than control cells following infection with these viruses. To study the role hGBP-1 plays in the IFN-mediated antiviral effect, cells were stably transfected with a construct expressing antisense RNA for hGBP-1. VSV infection of IFN-alpha-treated antisense RNA-expressing cells produced an amount of virus comparable to that produced in the parental cell line, while EMCV infection of the IFN-alpha-treated transfected cells and VSV and EMCV infection of the IFN-gamma-treated transfected cells produced far more virus than was produced in the parental cell line. These results demonstrate that GBP-1 mediates an antiviral effect against VSV and EMCV and plays a role in the IFN-mediated antiviral response against these viruses.
DNA-Binding Proteins↗
Reduced tumorigenicity of rodent tumour cells and tumour explants following infection with wild type and mutant herpes simplex virus, bovine mammillitis virus and encephalomyocarditis virus.
The tumorigenicity of neoplastic hamster and mouse cell lines and tumour explants was reduced by infection with herpes simplex virus (HSV-1), a thymidine-kinaseless mutant of herpes simplex virus, namely 'MDK', encephalomyocarditis virus (EMC) and bovine mammillitis virus (BMV). There was an approximate relationship between duration of virus infection in vitro and reduction in incidence and/or rate of tumour development. The rate of tumour development was also reduced by 'site inoculation' of virus (HSV-1) at various time intervals following inoculation of tumorigenic BHK 21 cells indicating that virus was capable of reducing the rate of tumour development in a situation where the neoplastic cells were already transplanted into the susceptible host species. It is suggested that the therapeutic role of wild type, mutant or recombinant viruses merits further exploration towards prevention and treatment of human cancer.
Animals↗
Detection by a solid phase independent enzyme immunoassay of monoclonal anti-idiotypic antibodies against monoclonal antibodies neutralizing Semliki Forest virus and encephalomyocarditis virus.
Neutralization inhibition enzyme immunoassay (NI-EIA) was evaluated for its usefulness to detect monoclonal anti-idiotypic antibodies (ab2mAbs) against idiotypic monoclonal antibodies (ab1mAbs) neutralizing either Semliki Forest virus (SFV) or encephalomyocarditis virus (EMCV). Purified ab1mAbs were coupled to keyhole limpet hemocyanin (KLH) mixed with the adjuvant Quil A and then injected intracutaneously into homologous BALB/c mice. Successful fusions were performed 5, 6 and 7 days after intracutaneous booster immunizations of these mice. Ab2mAbs in hybridoma supernatant fluids were detected by their capacity to block virus neutralization by ab1mAbs in NI-EIA. Two stable ab2mAb producing hybridomas were obtained against SFV neutralizing mAb UM 1.13, and twelve against EMCV neutralizing mAb UM 21.1.
Animals↗
Injection of mice with antibody to interferon renders peritoneal macrophages permissive for vesicular stomatitis virus and encephalomyocarditis virus.
Vesicular stomatitis virus (VSV) and encephalomyocarditis virus (EMCV) multiply in only a small percentage of peritoneal macrophages freshly explanted from 4- to 6-week-old male or female DBA/2, BALB/c, C3H, C57BL/6, or Swiss mice. However, when these mice were injected intraperitoneally with potent sheep (or goat) anti-mouse interferon alpha/beta globulin 4 days prior to harvesting peritoneal macrophages, the viruses multiplied to high titers and most of the cells were infected, as determined by total virus yield (VSV and EMCV), percentage of VSV antigen-positive cells (immunofluorescence), and determination of VSV infectious centers. This effect was not observed when mice were inoculated with other sheep hyperimmune or normal serum globulins. Anti-interferon globulin appeared to act in vivo because incubation of this globulin with peritoneal macrophages during the period of cell attachment or during the 18 hr after virus absorption did not render these cells permissive for VSV. Injection of mice with anti-interferon globulin did not affect the binding and uptake of labeled VSV by peritoneal macrophages. Although the underlying mechanism of this phenomenon is unknown, the results suggest that there may be low levels of endogenous interferon that contribute to host defense by maintaining some cells in an antiviral state.
Age Factors↗
Dissociation of interferon effects on murine leukemia virus and encephalomyocarditis virus replication in mouse cells.
Two subclones of Swiss mouse cells infected with Moloney murine leukemia virus (M-MuLV) were tested for their response to interferon (IFN). Whereas M-MuLV production in the two subclones was inhibited to the same extent, one of the subclones was significantly more sensitive to IFN when the antiviral effect was measured by replication of encephalomyocarditis (EMC) virus. The same subclone was also more sensitive to the anticellular activities of IFN. Additionally, NIH 3T3 cells infected with M-MuLV were completely resistant to IFN actions when EMC virus replication or the anticellular activities were tested. However, under the same conditions, M-MuLV production was completely inhibited by IFN. These results indicate that IFN may affect cell growth functions and EMC replication through mechanisms different from those by which MuLV production is inhibited.
Animals↗
Refractoriness of KB cell cultures carrying Japanese B encephalitis virus to encephalomyocarditis virus infection.
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Adenoviridae↗
Protection against herpes virus and encephalomyocarditis virus encephalitis with a double-stranded RNA inducer of interferon.
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Animals↗
Immunization of mice against encephalomyocarditis virus. I. Purification, concentration, and inactivation of encephalomyocarditis virus.
Methods are described for the concentration, purification, and inactivation of encephalomyocarditis virus grown in L-cell suspension cultures. Virus concentrates were obtained by the precipitation of crude virus lysates with polyethylene glycol and were purified by Genetron extraction. After column chromatography approximately 70% recovery of infectivity and hemagglutination (HA) activity was found. Exposure of the purified virus suspensions to ultraviolet light resulted in reduction of the infectivity by a factor of 10(9) with little or no loss of HA activity. The preparations are being evaluated as vaccines.
Animals↗
Evidence for a direct role for sialic acid in the attachment of encephalomyocarditis virus to human erythrocytes.
Sialic acid residues are required in cellular receptors for many different mammalian viruses. Sialic acid could have a direct role, being an integral part of the virus binding site on the receptor. Alternatively, negatively charged sialic acid could have an indirect role, being responsible for holding the receptor in the required configuration for virus recognition, for instance, by interacting with positively charged amino acid residues found in the polypeptide chain of receptors. We have investigated the role of sialic acid in virus attachment by studying the interaction of the small RNA virus encephalomyocarditis (EMC) with glycophorin A, its receptor on human erythrocytes. In several experiments, influenza virus A was used for control purposes. Blocking positive charges on glycophorin either in lysine residues by acetylation or in arginine residues with butanedione did not affect its interaction with EMC virus. In contrast, blocking negatively charged carboxyl groups in sialic acid residues by amidation destroyed the ability of glycophorin to inhibit EMC virus attachment suggesting an important role for this part of sialic acid in EMC virus attachment. Removal of the polyhydroxy side chain in sialic acid residues of glycophorin by mild oxidation with periodate followed by reduction with borohydride had little effect on its interaction with EMC virus. Further, sialic acid species with either an acetyl or glycolyl group attached to the amino group on position 5 interacted equally well with EMC virus.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylation↗