[Pathogenesis of mouse virus disease induced by CLM virus].
Explore the source record for details and available documents.
Animals↗
SEARCH · PubMed Health
Results for “VIRUS DISEASES”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Recent trends in the molecular diagnosis of infectious bursal disease viruses.
Infectious bursal disease virus (IBDV) causes an immunosuppressive disease in young chickens. Two serotypes of this double-stranded RNA virus exist but only serotype 1 viruses cause disease in chickens. Detection and strain identification of IBDV is important because antigenic subtypes found within serotype 1 make it necessary to tailor vaccination programs to the antigenic type found in the bird's environment. Because conventional virus isolation and characterization are not practical for routine diagnosis of IBDV, antigen-capture enzyme-linked immunosorbent assay (ELISA) and molecular assays based on reverse transcription-polymerase chain reaction (RT-PCR) technology were developed. Compared with antigen-capture ELISA, RT-PCR assays have greater versatility and are more sensitive and specific. Strain identification has been accomplished using a variety of post-RT-PCR assays, including restriction enzyme digestion of the RT-PCR products. The resulting restriction fragment length polymorphisms (RFLP) are used to differentiate viruses into molecular groups that correlate with antigenic and pathogenic types. Recently, two types of real-time RT-PCR have been used to identify and differentiate strains of IBDV. Both methods use distance-dependent interaction between two dye molecules, known as fluorescence resonance energy transfer (FRET). The dye molecules are attached to one or more nucleotide probes that detect specific nucleotide sequences of the virus. Our laboratory has used a two-probe assay to identify single-nucleotide mutations among IBDV strains. A mutation probe is used in this assay to detect substitution mutations in a region of the viral genome that encodes a neutralizing epitope of the virus. These assays are accurate, reliable and inexpensive compared with conventional RT-PCR because they do not require RFLP or other labor-intensive post-RT-PCR assays to distinguish viral strains.
Animals↗
Molecular cloning, expression and immunological analysis of the capsid precursor polypeptide (P1) from swine vesicular disease virus.
Swine vesicular disease virus (SVDV) is the aetiological agent of a highly contagious viral disease of pigs, whose symptoms are indistinguishable from those caused by foot-and-mouth disease virus (FMDV). The gene coding for the capsid protein precursor of SVDV (P1) from a recent spanish isolate (SPA/1/'93) was cloned and expressed in bacteria, and the antigenicity and immunogenicity of the recombinant product were evaluated. The recombinant P1 was recognised by antibodies against SVDV induced in pigs infected experimentally with different SVDV strains. Immunisation of swine with recombinant P1-induced SVDV-specific cellular and humoral immune responses. The implications of these results in SVD diagnostic as well as in vaccine development are discussed.
Animals↗
Formation, characterization and interfering capacity of a small plaque mutant and of incomplete virus particles of infectious bursal disease virus.
Serial undiluted passages of infectious bursal disease virus in chick embryo cells were accompanied by a von Magnus type fluctuation of infectivity in viral harvests and a gradual decrease of plaque size. From the 9th undiluted passage on, the whole virus population consisted of small plaque-forming virus. The small plaque size remained constant when subsequent infections were carried out at low multiplicities. Small plaque virus interfered with the replication of large plaque standard virus. The small plaque/low yield mutation favoured the generation of defective particles which could be separated from complete particles by their lower densities in CsCl-gradients, where six fractions became visible and could be analyzed separately. Most of the defective virus particles had lost the larger of their two dsRNA segments and showed an aberrant protein composition. They had a very low residual infectivity and were also able to interfere with the replication of complete virus.
Animals↗
Glycoprotein I of pseudorabies virus (Aujeszky's disease virus) determines virulence and facilitates penetration of the virus into the central nervous system of pigs.
In the present study we investigated the virulence and neural spread of pseudorabies virus (PRV) strains with mutations in the gene encoding glycoprotein I (gI) in 3-week-old pigs which were intranasally infected. Mutant M303 (lambda 125, 126) lacks amino acids valine-125 and cysteine-126 in an immunodominant antigenic region of gI which contains 2 discontinuous antigenic domains, whereas mutant virus M304 (lambda 59, 60) lacks amino acids glycine-59 and aspartic acid-60 in a continuous antigenic domain. Mutant M301 contains a frame shift mutation. Both mutants M301 (gI-) and M303 (lambda 125, 126) were not virulent for pigs, whereas mutant M304 (lambda 59, 60) was as virulent as wild-type PRV. All gI mutant viruses replicated in the oropharyngeal mucosa, although M304 (lambda 59, 60) and wild-type PRV replicated to higher titres than M303 (lambda 125, 126) and M301 (gI-). In contrast to M304 (lambda 59, 60) and wild-type PRV, both mutant viruses M301 (gI-) and M303 (lambda 125, 126) were not recovered from any part of the central nervous system at day 6 after infection. To study the spread of M301 (gI-) in the central nervous system in more detail, a second experiment was done in which 100-fold more virus was intranasally administered and virus was recovered from various tissues at day 4 after infection. Again, no gI-negative virus was isolated from the central nervous system. We concluded that deleting the amino acids valine-125 and cysteine-126 decreases virulence and reduces neurotropism to the same degree as deleting the gI protein. In addition, gI-negative virus does not spread in the central nervous system of pigs, probably because the transport of the virus across the synapse is hampered.
Animals↗
In ovo interference of embryo non-lethal avian infectious bronchitis viruses (IBV) with velogenic Newcastle disease virus and embryo adapted IBV.
Avian infectious bronchitis virus (IBV) interfered with the lethal effects of velogenic Newcastle disease virus (NDV) and embryo adapted IBV in eggs previously inoculated with non-lethal IBV. Greater interference was noted in eggs superinfected with embryo adapted IBV than velogenic NDV. The interference could be eliminated by treating the initial IBV with homologous anti-IBV serum.
Animals↗
[Utilization of poly U-cellulose and poly U-sepharose for the study of virus-specific RNA of Newcastle disease virus].
Comparative characteristics of poly(U)-cellulose and poly(U)-sepharose used for the study of virus-specific 18S RNA of Newcastle disease virus are presented. Upon chromatography of 18S NDV RNA on any of these columns, approximately 60-70% RNA was adsorbed. The sorbing RNA contained in poly(A) 10-12% of the total amount of adenosine, in contrast to RNA not adsorbed on the column in which poly(A) contained 1-2% of the total amount of adenosine in RNA molecule. The analysis in sucrose density gradient and polyacryl amide gel of the RNAs eluated from the columns showed RNA chromatography under the conditions used not to cause its degradation. The advantages and short-comings of the sorbents used in studies of virus-specific RNA are discussed.
Cellulose↗
Typing of the foot-and-mouth disease virus. Result of diagnosis and typing of foot-and-mouth disease virus.
Explore the source record for details and available documents.
Animals↗
Typing of the foot-and-mouth disease virus. Results of diagnosis and typing of foot-and-mouth disease virus.
Explore the source record for details and available documents.
Aphthovirus↗
[The neuropathogenesis of Borna disease virus infection].
Borna disease virus(BDV) is a noncytolytic, neurotropic RNA virus that causes a disease of the central nervous system(CNS) in several vertebrate species, including horses, sheep, cats and ostriches. Epidemiological studies using peripheral blood or brain samples revealed that BDV can infect humans and that it may be related with certain neuropsychiatric disorders. The unique genetic and biological properties of BDV indicate that BDV develops a persistent infection in the CNS. Furthermore, a line of recent evidences suggests that BDV infection causes direct effects on brain functions in the absence of immunopathology-related brain damage. In this review, we discuss about recent data regarding neuropathogenesis of BDV infections in animals and humans.
Animals↗
Induction of cell mediated immune response by nonspecific stimulator of immunity against antigenically unrelated oncogenic virus (Marek's disease virus).
An enzyme treated preparation of Mycobacterium phlei (NSI), induced strong cell mediated immune response (CMIR) against specific as well as against nonspecific oncogenic Marek's disease (MDV) in birds, as evinced by Lymphocyte migration inhibition, (LMIT) lymphocyte transformation test (LT) and Lymphokine (Lymphocyte migration inhibition factor) LyIF assay. Maximum CMIR could be observed towards third week post inoculation. All the three tests exhibited a positive correlation. Such phenomenon of CMIR induction by NSI, nonspecifically to unrelated viral/cancerous diseases (MD) in birds generates hopes for immunoprevention of these maladies by utilizing such phenomenon.
Adjuvants, Immunologic↗
Structure of infectious bursal disease virus.
Infectious bursal disease virus of chickens was purified, and its structure was examined by the negative-staining technique in the electron microscope. The buoyant density of infectious bursal disease virus in CsCl was found to be 1.34 g/cm(3). The morphological details suggest that the capsid of the virion consists of a single layer of 32 capsomeres arranged in 5:3:2 symmetry. The virion measured about 55 nm in diameter and had no envelope.
Animals↗
A necrotizing pneumonia in lambs caused by pseudorabies virus (Aujesky's disease virus).
An outbreak of pseudorabies occurred in sheep housed with swine in the same building. Although the sheep and swine were not in physical contact, the lambs and ewes were exposed to air from the sows' section. Three dead lambs were submitted to the Iowa State University Veterinary Diagnostic Laboratory for necropsy. Grossly there were pulmonary congestion and multifocal pulmonary hemorrhages. Microscopic lesions were severe acute multifocal necrotizing bronchopneumonia with necrotizing vasculitis and intranuclear inclusion bodies within the neurons of the parabronchial ganglia. Bacterial cultures were negative for pathogenic agents; pseudorabies virus was isolated from ovine brain tissue. Viral antigen was demonstrated in the neurons of the parabronchial ganglia by immunoperoxidase staining. Electron microscopy revealed nucleocapsids in the parabronchial ganglionic neurons which contained basophilic intranuclear inclusion bodies. Viral DNA prepared from the ovine pseudorabies virus isolate was found by restriction endonuclease analysis to be related to the Indiana Funkhauser strain of pseudorabies virus.
Animals↗
[Behavior of foot and mouth disease virus for adsorption in aluminum hydroxide and subsequent elution. III. Purification and concentration of foot and mouth disease virus through aluminum hydroxide].
Explore the source record for details and available documents.
Adsorption↗
Intracellular processing of the vesicular stomatitis virus glycoprotein and the Newcastle disease virus hemagglutinin-neuraminidase glycoprotein.
The kinetics of intracellular transport of the vesicular stomatitis virus (VSV) glycoprotein (G) and the Newcastle disease virus (NDV) hemagglutinin-neuraminidase (HN) glycoprotein in chicken embryo cells were compared. To assay for the appearance of pulse-labelled glycoprotein at the cell surface, an antibody-binding assay was developed which allowed the precipitation of only those molecules on the outside surfaces of infected cells. Using this assay, it was found that pulse-labelled VSV G protein appeared at the cell surface with a half-time of approximately 27 min, while pulse-labelled NDV HN glycoprotein reached the cell surface with a half-time of approximately 78 min. To determine the transit time of these glycoproteins to trans-Golgi membranes, the kinetics of the acquisition of endoglycosidase H resistance was analyzed. The half-time of the transit of the G protein to the trans-Golgi membranes was found to be approximately 13 min while that of the HN glycoprotein was found to be approximately 60 min. Since the G protein migrates to the trans-Golgi membranes with a half-time of 13 min, and the cell surface with a half-time of 27 min, the half-time for the transit between the trans-Golgi membrane and the plasma membrane must be approximately 14 min. In a similar analysis, the half-time for the transit of the HN glycoprotein from the trans-Golgi membrane to the plasma membrane must be approximately 18 min, a time not significantly different from that of the G protein. Thus the difference in the kinetics of the intracellular transport of these two glycoproteins resides primarily in the transit from the rough endoplasmic reticulum to the trans-Golgi membranes. These results argue against a non-selective mechanism for the transport of plasma membrane glycoproteins to the cell surface.
Animals↗
Foot-and-mouth disease virus: biology and prospects for disease control.
Foot-and-mouth disease virus (FMDV) is the causative agent of a disease that constitutes one of the main animal health concerns, as evidenced by the devastating outbreaks that occurred in different areas of the world over the last few years. In this review, we summarise important features of FMDV, aspects of its interactions with cells and hosts as well as current and new strategies for FMD control by vaccination.
Animals↗
Effect of infectious bursal disease virus on protection against Marek's disease by turkey herpesvirus vaccine.
Chickens inoculated at hatch with pathogenic infectious bursal disease virus (IBDV) and the turkey herpesvirus (HVT) vaccine were poorly protected against challenge at 1 week with virulent Marek's disease virus (MDV). However, if vaccination with HVT preceded IBDV inoculation such as by embryonal vaccination with HVT and exposure to IBDV at hatch, or by vaccination at hatch and IBDV exposure 5 days or longer postvaccination, then the vaccinal efficacy of HVT was not influenced. Further, the inhibitory effect of pathogenic IBDV was transient: chickens that received IBDV and HVT at hatch were poorly protected against challenge with virulent MDV at 1 week but not against challenge at 2 weeks of age. Pathogenic IBDV routinely interfered in vaccine efficacy of HVT in chickens lacking maternal antibody to IBDV but not in chickens that had such antibodies at the time of exposure to IBDV. In certain experiments, pathogenic IBDV caused a high rate of mortality in newly hatched chicks. Chickens receiving IBDV and MDV had a lower incidence of Marek's disease than those receiving MDV alone.
Animals↗
Antigenic structure of the capsid protein of rabbit haemorrhagic disease virus.
Rabbit haemorrhagic disease virus (RHDV) causes an important disease in rabbits. The virus capsid is composed of a single 60 kDa protein. The capsid protein gene was cloned in Escherichia coli using the pET3 system, and the antigenic structure of RHDV VP60 was dissected using 11 monoclonal antibodies (MAbs) and 12 overlapping fragments of the protein expressed in E. coli. Two antigenic regions were found. Ten out of the 11 MAbs recognized different discontinuous epitopes in the most immunodominant region of the viral capsid. This domain was located between residues 31 and 250 of the VP60 N terminus. The other MAb revealed the presence of an antigenic site within 102 aa of the C terminus. This MAb did not recognize the major cleavage product of the full-length 60 kDa protein. These results indicate that, in contrast to other caliciviruses such as Norwalk virus (NV), the 36 kDa cleavage product probably forms the N-terminal region of VP60. However, as in NV, the cleavage region appears to be the most immunodominant region.
Animals↗