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Gangliosides as paramyxovirus receptor. Structural requirement of sialo-oligosaccharides in receptors for hemagglutinating virus of Japan (Sendai virus) and Newcastle disease virus.

A sensitive assay system for receptor activity of gangliosides to paramyxovirus was developed. This system involves incorporation of gangliosides into neuraminidase-treated chicken erythrocytes (asialoerythrocytes) followed by estimation of virus-mediated agglutination and hemolysis. The asialoerythrocytes coated with I-active ganglioside (Sia alpha 2-3Gal beta 1-4GlcNAc beta 1-3(Gal alpha 1-3Gal beta 1-4GlcNAc beta 1-6)Gal beta 1-4GlcNAc beta 1-3Gal beta 1-4Glc beta 1-Cer) were effectively agglutinated by hemagglutinating virus of Japan (HVJ, Sendai virus). The hemolysis of the asialoerythrocytes mediated by HVJ was restored to the highest level by labeling the cells with gangliosides possessing lacto-series oligosaccharide chains, i.e., I-active ganglioside, N-acetylneuraminosylparagloboside (SiaPG(NeuAc)), and i-active ganglioside (Sia alpha 2-3Gal beta 1-4GlcNAc beta 1-3Gal beta 1-4GlcNAc beta 1-3Gal beta 1-4Glc beta 1-Cer). The specific receptor activity of ganglioside GD1a possessing a gangliotetraose chain was lower than those of the gangliosides described above. Gangliosides GM3, GD3, GM1a, GD1b, SiaPG(NeuGc) showed little effect on the restoration of HVJ-mediated hemolysis. On infection with Newcastle disease virus (NDV), the highest specific restoration of lysis was found in chicken asialoerythrocytes coated with SiaPG(NeuAc or NeuGc) and GM3(NeuAc or NeuGc), whereas those coated with I-active ganglioside, GD3, GM1a, and GD1b showed very low NDV-mediated hemolysis. The above results indicate that the determinants of receptor for HVJ contain sialylated branched and/or linear lacto-series oligosaccharides carried by I,i-active gangliosides and SiaPG(NeuAc) and sialosylgangliotetraose chain carried by GD1a. The determinants for NDV are carried by SiaPG(NeuAc or NeuGc) containing linear lacto-series oligosaccharide and GM3(NeuAc or NeuGc). The absence of detectable binding of free oligosaccharides obtained from I-active ganglioside and sialoglycoprotein GP-2 isolated from bovine erythrocyte membranes as HVJ receptor (Suzuki, Y., et al. J. Biochem. (1983) 93, 1621-1633; (1984) 95, 1193-1200) indicates that HVJ recognizes the sialooligosaccharides oriented out of the lipid bilayer in the cell membranes where the hydrophobic ceramide or peptide backbone of the receptor is integrated.

Animals↗

Protection conferred by vaccination with Blacksburg and Komarov strains of Newcastle disease virus against Newcastle disease in Bangladesh.

An evaluation was undertaken of the efficacy of vaccination of day-old chicks with the Blacksburg (B1) strain of Newcastle disease virus (NDV) followed at various times by vaccination with the Komarov (K) strain. Antibody was detected by the haemagglutination inhibition (HAI) test one week after vaccination with B1 and titres peaked at three weeks and had declined to undetectable levels by nine weeks. After subsequent vaccination with K strain at five, seven or eight weeks of age levels of HAI antibody (titre 80 to 640) were detected after three weeks. Birds vaccinated at seven weeks were tested for antibody and resistance to challenge beyond 19 weeks of age. In this group the HAI titres remained constant (80 to 640) up to 32 weeks of age and then steadily declined to 10 to 20 at 44 weeks of age. A linear relationship between HAI titre and virus neutralising index (VNI) was demonstrated with a range of selected sera. Only birds with an HAI titre of 80 or greater resisted artificial challenge. It is recommended that, following B1 vaccination at day-old and K vaccination at seven weeks old, revaccination with K strain should be performed at intervals of not more than seven months.

Animals↗

A serological survey of antibodies to rabbit haemorrhagic disease virus (rabbit calicivirus disease) in two rural Central Otago communities.

AIMS: To determine whether individuals from two rural communities with heavy exposure to the Rabbit Haemorrhagic Disease Virus (RHDV) developed antibodies to this virus. METHODS: Sera were assayed using competition ELISA (cELISA) and solid phase ELISA (spELISA). Exposure estimates were based on answers to an interviewer administered questionnaire. RESULTS: Of the 104 participants, 79 were considered to have experienced high or medium exposure, many of whom described specific exposures. There were 58 people who reported contact with RHDV infected bait, organ homogenate mixtures or rabbit body fluids. A one-way analysis of variance (Kruskal Wallis) found that human cELISA results were differently distributed from both strongly RHDV positive rabbits (chi2(1) = 27.37, p < 0.001) and weakly RHDV positive rabbits (chi2(1) = 27.35, p < 0.001). The distribution of assay results in each exposure group did not differ in either cELISA (chi2(2) = 2.49, p = 0.29) or spELISA (chi2(2) = 1.70, p = 0.43). Relatively fewer results were categorised as reactive (two 'barely' positive and two doubtful) than in a previous survey of 493 unexposed people. None of the five positive results categorised by the less specific spELISA occurred in people described as 'barely' positive or doubtful by cELISA. CONCLUSIONS. No serological evidence of infection with RHDV was found in a cohort including many heavily exposed individuals.

Adult↗

Lack of contact transmission of recombinant Marek's disease virus type 1 expressing the fusion protein of Newcastle disease virus.

To clarify the level of excretion of a recombinant Marek's disease virus type 1 (rMDV1) that confers good protection in chickens against both Marek's and Newcastle diseases, even in the presence of maternal antibodies, contact transmission tests were conducted. Naïve chickens kept in the same cage or room with chickens inoculated with rMDV1 did not produce antibodies against MDV1 or the fusion protein of Newcastle disease virus. Moreover, the rMDV1 was not isolated from the dander of chickens inoculated with rMDV1. Even under the stressful conditions of forced molting and a high temperature environment, rMDV1 was not isolated from the dander of inoculated birds. The viral DNA, however, was detected from the dander of chickens inoculated with rMDV1 as well as a commercial vaccine. These findings indicate that dander from chickens inoculated with rMDV1 includes viral DNA, but does not contain infectious virus.

Animals↗

[The development of a purification method for Borna disease virus].

Borna disease virus represents an unknown neurotropic agent. It causes encephalitis in horses and sheep. The same or a similar type of virus might be responsible for psychiatric disorders in man. So far, it has been impossible to purify this agent to such an extent that it could be analyzed biochemically or electronmicroscopically. Therefore, different conventional virus purification techniques are applied in order to develop a method for obtaining purified Borna disease virus from infectious rat brain or persistently infected cell culture material.

Animals↗

Herpesvirus of turkey recombinant viruses expressing infectious bursal disease virus (IBDV) VP2 immunogen induce protection against an IBDV virulent challenge in chickens.

Two recombinant herpesviruses of turkey (HVT) expressing the VP2 protein of infectious bursal disease virus (IBDV or Gumboro disease virus) have been constructed: vHVT001 and vHVT002. The VP2 open reading frame was inserted at the locus of the small subunit of ribonucleotide reductase gene (HSV-1 UL40 homolog) without any exogenous promoter in vHVT001 and at the locus of gl gene (HSV-1 US7 homolog) under the control of the human cytomegalovirus immediate-early promoter in vHVT002. The isolation of these recombinant viruses indicated that the deleted genes were not required for replication of HVT in chicken embryo fibroblasts. Efficacy of these recombinant viruses against IBDV strain 52/70 and Marek's disease virus (MDV strain RB1B) virulent challenges was evaluated in chickens vaccinated at 1 day of age. In the IBDV challenge, a good protection against mortality and bursal gross lesion was observed in vHVT002-vaccinated chickens: 100% with 10(5) PFU dose and 60% with 10(4) PFU dose; in contrast, only a weak level of protection was achieved after vaccination with vHVT001. Protection levels against MDV challenge obtained with vHVT001 and vHVT002 were low (around 10%) compared to that induced by the parental HVT (84%). In spite of the low protection level against MDV, this is the first report which describes induction of full protection against IBDV with a single inoculation of a recombinant virus.

Animals↗

Identification of a nonvirion protein of Aleutian disease virus: mink with Aleutian disease have antibody to both virion and nonvirion proteins.

We studied Aleutian disease virus polypeptides in Crandall feline kidney (CRFK) cells. When CRFK cells labeled with [35S]methionine at 60 h postinfection were studied by immunoprecipitation with sera from infected mink, the major Aleutian disease virus virion polypeptides (p85 and p75) were consistently identified, as was a 71,000-dalton nonvirion protein (p71). The peptide maps of p85 and p75 were similar, but the map of p71 was different. p85, p75, and p71 were all precipitated by sera from Aleutian disease virus-infected mink, including those with signs of progressive disease, but heterologous sera raised against purified Aleutian disease virus did not precipitate the nonvirion p71. These results indicated that the nonvirion p71 was unrelated to p85 and p75 and further suggested that mink infected with Aleutian disease virus develop antibody to nonvirion, as well as structural, viral proteins.

Aleutian Mink Disease↗

Borna disease virus.

Borna disease virus, a negative-strand RNA virus, infects a wide variety of warm-blooded animals. Depending on the age of the host and the integrity of its immune response, infection may be asymptomatic or cause a broad spectrum of behavioral disorders. Unusual features of Borna disease virus biology include nuclear localization of replication and transcription; diverse strategies for regulation of gene expression; and interaction with signaling pathways resulting in subtle neuropathology. Although the question of human infection remains unresolved, burgeoning interest in this unique pathogen has provided tools for exploring the pharmacology and neurochemistry of neuropsychiatric disorders potentially linked to infection. Analysis of rodent models of infection has yielded insights into mechanisms by which neurotropic agents and/or immune factors may impact developing or mature central nervous system circuitry to effect complex disturbances in movement and behavior.

Animals↗

Effect of temperature on radiosensitivity of Newcastle disease virus.

Newcastle disease virus was irradiated at temperatures ranging from 2.2 to 60 C. An interaction between the thermal and ionizing energy was observed in the temperature region of 49 to 60 C. At 2.2 C, the hemagglutinin was considerably more radioresistant than the infectivity property. It is believed that radiation inactivation of Newcastle disease virus infectivity at low temperatures was due to nucleic acid degradation and at higher temperatures was due to protein denaturation.

Antibodies↗

Quantitative basic residue requirements in the cleavage-activation site of the fusion glycoprotein as a determinant of virulence for Newcastle disease virus.

Newcastle disease virus exhibits a wide range of pathogenicity and virulence which, as with all paramyxoviruses, is directly related to the cleavability of a precursor (F0) of the fusion glycoprotein by cellular proteases. Sequence analyses of the cleavage site of several virulent and avirulent isolates of the Newcastle disease virus serotype reveal a correlation between virulence or pathogenicity and a high content of basic amino acid residues at the cleavage site. A similar correlation has been seen for other paramyxoviruses.

Amino Acid Sequence↗

Isolation and characterization of defective interfering particle of Newcastle disease virus.

Newcastle disease virus grown in embryonated eggs was separated and purified by sucrose density gradient centrifugation into two distinct type of particles, B and T, the former being normal virus particles with high activities of hemagglutination, hemolysis, neuraminidase and infectivity, the latter being non-infectious virus particles with low activities of hemolysis and neuraminidase but high hemagglutination activity. B and T particles were shown to share a common antigen by immunodiffusion test. T particles were deficient in viral RNA, since they contained only 13s RNA in a small amount, whereas B particles possessed a large amount of 57s RNA and a small amount of 13s RNA. T particles interfered with the multiplication of normal Newcastle disease virus in primary cultures of chick embryo cells.

Animals↗

Molecular anatomy of lymphocystis disease virus.

Lymphocystis disease (LD) has been reported to occur in over one hundred different species of fish worldwide. The disease is caused by lymphocystis disease virus (LCDV), a member of the iridovirus family. Numerous fish species that play an important role in fishery and fish farming are highly susceptible to LCDV infection. The infected animals develop disseminated clusters of aberrant hypertrophied cells within their connective tissue, the so-called lymphocystis cells. In the cytoplasm of these cells a massive accumulation of virions can be observed. As a first step towards understanding the mechanisms of viral infection and pathogenesis the complete genomic nucleotide sequence of lymphocystis disease virus type 1 (LCDV-1; flounder isolate) was determined. LCDV-1 is the type species of the genus Lymphocystivirus within the family Iridoviridae. The virions contain a single linear double-stranded DNA molecule that is circularly permuted, terminally redundant and heavily methylated. Since there is no convenient cell system for virus replication we determined the complete nucleotide sequence of the viral genome (102,653 base pairs). Computer assisted analyses of 195 potential open reading frames resulted in the identification of a number of putative gene products with significant homology to functionally characterized proteins of other species.

Animals↗

Induction of mucosal disease in cattle persistently infected with noncytopathic bovine viral diarrhea-mucosal disease virus by superinfection with cytopathic bovine viral diarrhea-mucosal disease virus.

Three head of cattle persistently infected with noncytopathic bovine viral diarrhea-mucosal disease virus (ncBVD-MDV) were superinfected naturally or experimentally with cytopathic bovine viral diarrhea-mucosal disease virus (cBVD-MDV). In the naturally superinfected case, one animal manifested pyrexia and severe diarrhea, and died without developing antibodies to cBVD-MDV. However, another animal survived with only continual slight anorexia and pyrexia, and developed strong resistance to the superinfected strain. In the experimental cases, induction of MD was unsuccessful in two persistently infected cattle when superinfected with cBVD-MDV antigenically heterologous for persistently infected ncBVD-MDV. They also developed antibodies to the cBVD-MDV strain with which they had been infected. After 6 months, these cattle were infected again with a cBVD-MDV strain different from that used in the previous experiment. One animal infected with this strain, which was antigenically homologous to the persistently infected strain, died after developing MD symptoms without developing antibodies to the infecting strain. It is suggested that the antigenic relationship between the persistent ncBVD-MDV and the superinfected cBVD-MDV was an important factor in developing MD.

Animals↗

Avian cells expressing the Newcastle disease virus hemagglutinin-neuraminidase protein are resistant to Newcastle disease virus infection.

The cDNA derived from the Newcastle disease virus (NDV) hemagglutinin-neuraminidase (HN) gene was inserted into a replication-competent Schmidt-Ruppin Rous sarcoma virus-derived vector. Chick embryo cells transfected with this vector expressed HN-sized protein which could be precipitated with anti-HN antibody. These cells adsorbed avian red blood cells and the cell surfaces exhibited neuraminidase activity while cells transfected with an antisense version of the gene were negative for hemadsorption and neuraminidase. The cells transfected with the retroviral vector containing the HN gene were resistant to infection by NDV and influenza virus, viruses which bind to sialic acid containing receptors, but sensitive to vesicular stomatitis virus (VSV). Cells transfected with the antisense version of the HN gene were sensitive to NDV, influenza virus, and VSV infection. Thus the HN protein-expressing cells are likely resistant to NDV and influenza virus due to the destruction of the cellular receptors by the neuraminidase of the HN protein. The expression of the influenza virus HA protein using the same retrovirus vector has been reported previously (L. A. Hunt, D. W. Brown, H. L. Robinson, C. W. Naeve, and R. G. Webster, 1988, J. Virol. 62, 3014-3019). Cells infected with this vector were sensitive to infection with influenza virus, NDV, and VSV. Thus expression of a viral surface protein does not necessarily confer resistance of the cell to the homologous virus.

Animals↗