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Results for “avian viruses”

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At least 19 recordsLinked to original sources
PubMed1979

The sensitivity of some avian viruses to formaldehyde fumigation.

Various avian viruses (infectious bursal agent, reovirus, adenovirus, infectious bronchitis, Newcastle disease, poxvirus, avian encephalomyelitis and infectious laryngotracheitis virus) as suspensions in buffer or in a litter slurry were exposed to aerosolized formalin in an attempt to determine the efficacy of this fumigation method for decontamination of laboratory isolation cubicles. Formalin (37% formaldehyde) was delivered by a commercial insecticide fogger at a flow rate of 40 ml per minute and a volume of 36 ml per cubic meter of space. Fumigated cubicles were left sealed for 18 hr (cycle 1) before viruses were sampled, or were then exposed to a second fumigation and left sealed for an additional six hour period (cycle 2) before viruses were titrated (commencing at a 1:10 dilution) for residual infectivity. Although the infectivity of all viruses was reduced by over 99% by one fumigation cycle, the second cycle was necessary for reduction of Newcastle disease and reoviruses to non-detectable (no infectivity demonstrated in a 1:10 dilution of fumigated virus) levels.

Animals↗
PubMed1975

Evidence for a host cell surface antigen on the envelope of avian tumour viruses.

Avian sarcoma viruses of the A, B, C, D and E subgroups are inactivated about 100-fold by the serum of rabbits immunized against chick embryo (CE) cells, in the presence, but not in the absence, of complement. The inactivation is not due to the action of the antiserum and complement on the CE cell cultures used for virus assay, nor to anti-Forssman antibodies, but it is presumably due to antibodies to some antigen(s) common to the surface of CE cells and to the virus envelope. This host cell surface antigen (HSCA) is also present on the surface of the helper viruses RAV1 and RAV2 of Bryan strain Rous sacroma virus. However, it cannot be said whether it is identical for viruses of all subgroups. A parallel electron microscopical study has revealed a characteristic swelling and loss of opacity to electrons of virus particles treated with the antiserum and complement, which appears to precede virolysis. Avian sarcoma viruses are not inactivated, in the presence or absence of complement, by antiserum to BHK21 hamster cells transformed by RSV and carrying virus-induced surface antigen (VISA). Therefore, the virus particles do not carry any surface antigen common to transformed non-permissive and permissive cells.

Animals↗
PubMed1976

Identification of DNA in the core component of avian myeloblastosis virus.

Avian myeloblastosis virus (AMV) was found to contain DNA associated with the virion. The viral envelope was removed by treating the virus with a nonionic detergent and the DNA was found in the core fraction. These experiments indicate that the DNA associated with tumor virus is not contaminant associated with the viral envelope and suggest that the DNA is part of the internal core component. The DNA from avian myeloblastosis virus has a density of 1.70 g/cm3.

Avian Leukosis Virus↗
PubMed1978

Fractionation of proteins from Rous sarcoma virus and avian myeloblastosis virus by isoelectric focusing.

The isoelectric focusing technique in the pH gradients was used for a preparative isolation of proteins from Rous sarcoma virus and avian myeloblastosis virus. The purified major gs protein, p27 (pI = 9.1) and the gP86 (pI = 5.3) were obtained after disruption of virus with 1% non-ionogenic detergent in the presence of 6M urea. The p10, p15, and p19 were present in the same range of pH (pI = 6.8). A strongly basic protein, immunologically active, presumably the p12, was found in the alkaline region of the pH gradient 10.8. These proteins fully retained their immunological activity. On the other hand, in the acidic region of the pH gradient between pH 4 and 5, strong precipitates were regularly found. These precipitates were complexes which were formed by interaction of the acid components of ampholines with the viral proteins during isoelectric focusing. Almost all viral proteins were present, differing only in quantity. The complexes were stabile in 1% non-inogenic detergent and 6M urea. They were dissociated with 1% SDS and 5M urea, and had no immunological activity. The methods of virus disruption and possibilities of formation of the ampholine-viral protein complexes are discussed.

Avian Leukosis Virus↗
PubMed1977

Characterization of tumour virus proteins. I. Radioimmunoassay of the P27 protein of avian viruses.

The major structural protein of avian oncornaviruses, a core component of about 27000 daltons, has been measured by radioimmunoassay. The purified protein was labelled with 125Iodine by chloramine-T method. The immune serum titer was defined as the highest serum dilution able to precipitate 50% of the labelled antigen present in the system. Standard competition curve was constructed in order to determine the equivalents of protein, in a system with limiting antibody concentration. In the experimental conditions used, 0.14 ng of AMV-P27 inhibited 50% of 125I-AMV-P27 (1.0 ng) precipitation. The 125I-AMV-P27 vs anti-AMV-P27 system was used to study the competition of normal cells, purified virus suspension, productive cells and supernatant fluids. Most of the chicken embryo fibroblasts showed expression of this viral component. The phenomena of cell transformation, the increase in total protein, and the expression of P27 were studied in rapid transformation of CEF by RSV-SRA.

Alpharetrovirus↗
PubMed1977

The inhibition of Rauscher leukemia virus and avian myeloblastosis virus DNA polymerases by anthracycline compounds.

Studies by other investigators have shown that adriamycin and daunorubicin exhibit antitumor and antiviral activity. A possible antiviral mechanism for the anthracycline compounds is the potent inhibition of viral DNA polymerases. Five anthracycline compounds were tested against purified Rauscher leukemia virus and avian myeloblastosis virus DNA polymerases. All compounds were found to be potent inhibitors of viral DNA polymerase activity. Inhibition was found to be primarily due to the planar ring structure (daunomycinone) common to all of these compounds. The degree of inhibition was dependent on the templates used: activated DNA, synthetic hybrids, poly(rA).dT12-18 and poly(rC).dG12-18, and the synthetic copolymer, poly(DA-dT). Alteration of the group substituent on the planar ring affected the degree of viral DNA polymerase inhibition. The inhibitory effects by anthracycline compounds appear to be relatively specific for viral polymerases.

Anthracenes↗
PubMed1978

High-molecular-weight RNAs of AKR, NZB, and wild mouse viruses and avian reticuloendotheliosis virus all have similar dimer structures.

Several 50 to 70S tumor viral RNAs have previously been shown by electron microscopy to be dimers, with the two monomer subunits joined near their 5' ends. Five additional naturally occurring type C RNA tumor viruses have now been examined: AKR, and endogenous murine ecotropic virus; NZB, an endogenous murine xenotropic virus; and ecotropic and an amphotropic virus isolated from a wild mouse; and the avian reticuloendotheliosis virus (REV). All five 50 to 70S RNAs have similar 5'-to-5' dimer structures. Therefore, the observations support the hypothesis that the dimer linkage is a structural feature common to all type C mammalian viruses. REV is the first example of an avian virus with a clear 5'-to 5' dimer linkage. All of the mammalian viral RNAs, but not REV, showed symmetrically placed loops in each subunit of the dimer. Possible molecular structures and biological functions of the dimer linkages and loops are discussed.

AKR murine leukemia virus↗
PubMed2025

Mammalian antiviral proteins ZAP and KHNYN can independently restrict CpG-enriched avian viruses.

Zoonotic viruses are an omnipresent threat to global health. Influenza A virus (IAV) transmits between birds, livestock, and humans. Proviral host factors involved in the cross-species interface are well known. Less is known about antiviral mechanisms that suppress IAV zoonoses. We observed CpG dinucleotide depletion in human IAV relative to avian IAV. Notably, human ZAP selectively depletes CpG-enriched viral RNAs with its cofactor KHNYN. ZAP is conserved in tetrapods, but we uncovered that avian species lack KHNYN. We found that chicken ZAP may not affect IAV (PR8) or CpG-enriched IAV (PR8CG). Human ZAP or KHNYN independently restricted CpG-enriched IAV PR8CG by overexpression in chicken cells and by combined knockout in human cells. Additionally, mammalian ZAP-L and KHNYN also independently restricted an avian retrovirus (ROSV). Curiously, platypus KHNYN, the most divergent from eutherian mammals, was also capable of independent restriction of multiple diverse viruses. We suggest that some mammalian KHNYN can act as a bona fide restriction factor with cell-autonomous activity. Furthermore, we speculate that through repeated contact between avian viruses and mammalian hosts, protein changes may accompany CpG-biased mutations or reassortment to evade mammalian ZAP and KHNYN.

Animals↗
PubMed1975

Comparison of an avian osteopetrosis virus with an avian lymphomatosis virus by RNA-DNA hybridization.

Myeloblastosis-associated virus (MAV)-2(0), a virus which was derived from avian myeloblastosis virus and induced a high incidence of osteopetrosis, was compared with avian lymphomatosis virus 5938, a recent field isolate which induced a high incidence of lymphomatosis. The following information was obtained. (i) MAV-2(0) induced osteopetrosis, nephroblastoma, and a very low incidence of hepatocellular carcinoma. No difference was seen in the oncogenic spectrum of end point and plaque-purified MAV-2(0). (ii) 125I-labeled RNA sequences from MAV-2(0) formed hybrids with DNA extracted from osteopetrotic bone at a rate suggesting five proviral copies per haploid cell genome. The extent of hybridization of MAV-2(0) RNA with DNA from osteopetrotic tissue was more extensive (87%) than was observed in reactions with DNA from uninfected chicken embryos (52%). (iii) Competition of unlabeled viral RNA in hybridization reactions between the radioactive RNA from the two viruses and their respective proviral sequences present in tumor tissues showed that 15 to 20% of the viral sequences detected in these reactions were unshared. In contrast, no differences were detected in competition analyses of RNA sequences from the two viruses detected in DNA of normal chicken cells. (iv) MAV-2(0) 35S RNA was indistinguishable in size from avian lymphomatosis virus 5938 35S RNA by polyacrylamide gel electrophoresis.

Animals↗
PubMedDate not supplied

Rapid diagnosis of some avian virus diseases.

Direct electron microscopy was used to identify virions of infectious laryngotracheitis in lysed tracheal cells and of fowlpox in scabs and exudates from natural cases. Rapid identification of avian adenovirus and infectious laryngotracheitis by gel diffusion was possible using antigens prepared by simple distilled-water lysis of infected cell cultures. Precipitin lines were often visible within 5 hours.

Animals↗
PubMedDate not supplied

[Sensitivity of Japanese quail, embryos and embryonal tissue culture to infection with several avian viruses].

The sensitivity of the biological system Japanese quail-embryo-quail fibroblast cultures to some common fowl viruses (Newcastle disease virus, infectious laryngotracheitis and infectious bronchitis viruses) was studied. Japanese quails, their embryos and embryo cell cultures were found to be sensitive to Newcastle disease virus infection. The virus reproduction was accompanied by death of embryos and destruction of cell culture. Japanese quails are sensitive to infectious laryngotracheitis virus given as aerosol. Reproduction of this virus in embryos was accompanied by formation of plaques on the chorioallantoic membrane and in the cell cultures by incomplete cytopathic effect. Japanese quails were found to be sensitive to infectious bronchitis virus, while their embryos and embryo cell cultures had low susceptibility to this virus.

Animals↗