Newcastle disease virus infected

Hand, R., 1976, Thymidine metabolism and DNA synthesis in Newcastle disease virus-infected cells, J. Virol. 19 801. 

Kara T, Endo T, Furukawa K, Kawakita M. Kobata A. Elucidation of the phenotypic change on the surface of Had-1 cell, a mutant cell line of mouse FM3A carcinoma cells selected by resistance to Newcastle disease virus infection. J. Biochem. (Tokyo) 1989 706 236-247. 

Inhalation 50 48 h Exposure increased infection rate with Newcastle disease virus. LOAEL 50 Anderson et al. 1964... 

Anderson, D.P., C.W.Beard, and R.P.Hanson. 1964. The adverse effects of ammonia on chickens including resistence to infection with Newcastle disease virus. Avian Dis. 8 369—379. Appelman, L.M., W.F.ten Berge, and P.GJ.Reuzel. 1982. Acute inhalation toxicity study of ammonia in rats with variable exposure periods. Am. Ind. Hyg. Assoc. J. 43(9) 662-665. ATSDR (Agency for Toxic Substancs and Disease Registry). 1990. Toxicological Profile for Ammonia. Prepared by Syracuse Research Corporation, for U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry. December. 

Castanospermine has been screened for efficacy against simian immunodeficiency virus (265), and has been shown to prevent syncytium formation in feline astrocyte cultures infected with the feline immimodeficiency virus by modifying the viral cell envelope (266). It suppressed syncytium formation and hemolytic activity in baby hamster kidney cells infected with Newcastle disease virus however, synthesis and cell surface expression of the hemagglutinin-neuraminidase glycoprotein in the viral envelope were not affected, which strengthens the hypothesis that poor transport of the parent alkaloid across membrane barriers may limit its therapeutic use (267). Both 239 and its 6-0-butanoyl ester had comparable relative toxicities and antiviral effects on Rauscher murine leukemia virus (268), but the ester was more potent than the parent alkaloid in inhibiting replication of Moloney murine leukemia virus (258). The ester was also active against herpes simplex viruses types 1 and 2 (269,270). In the latter case, conclusive evidence was provided for intracellular hydrolysis to 239. 

Infectious Diseases. Resistance to a variety of organisms, including BCG, cryptococcus, and Candida, has been shown to be increased in immunosuppressed animals following in vivo treatment with TF5 (Collins and Auclair, 1979 Collins and Morrison, 1979 Bistoni et al., 1982 Ishitsuka et al, 1983). The basis for this increased resistance may be explained by studies showing that mouse strains with low resistance to Candida or BCG have increased resistance and elevated production of two lymphokines, MIF and 7 interferon following in vivo treatment with TF5 (Neta and Salvin, 1983 Salvin and Neta, 1983). Similar results were seen with Taj. In another model, interferon production in response to Newcastle s disease virus infection was also increased by in vivo treatment with TF5 or Ta (Huang et al., 1982). 

Human fibroblast and leukocyte interferons show a strong affinity for the copper chelate of bis-carboxymethylaminoagarose. Human leukocyte interferon adsorbs non-specifically to immobilized hyperimmune serum immunoglobulin The interferon can be recovered by washing the adsorbent with 1,2-dihydroxyethane. An improved procedure for the isolation of interferons produced by mouse Ehrlich ascites tumour cells infected with Newcastle disease virus provides interferons of three size classes (mol. wts. 3.3 X lO", 2.6x10, ... 

Youssef (1996) found that the mortahty rate in chickens infected with a virulent Newcastle disease virus was significantly enhanced with Pb dosing (20 or 40 mg/kg/day at 1—56 days). A vaccine for the virus decreased the mitogenic response in lymphocytes. 

One of the problems encountered in studies of viral cytopathic effects is to quantitate the number of cells undergoing changes or dying. Some indication of the number of cells involved can be obtained by estimating those that fail to exclude dyes because of altered membrane impermeability. A more accurate, but somewhat tedious technique was designed by Marcus and Puck (1958). These authors devised a means to study quantitatively the destruction of mammalian cell reproductive capacity by scoring the fraction of monodisperse HeLa cells infected with Newcastle disease virus to survive and form colonies over a period of 8-10 days incubation. They concluded that one virus particle was sufficient to kill a single cell. This method has been extended to other viruses by Marcus (1959) and can be used to... 

The paramyxoviruses, largely because of their profound cell-fusing activity, have served as an important model of membrane perturbation by viruses. During Sendai virus-mediated fusion of mouse ascites cells, Pasternak and Micklem (1973) detected loss of intracellular metabolites coincident with inhibition of their accumulation from the medium. This failure to maintain selective permeability did not occur at 0°C and was unaffected by cytochalasin B which inhibits fusion by the virus. Chick embryo fibroblasts infected with Newcastle disease virus were found to release cellular enzymes, such as lactate dehydrogenase, glutamic oxaloacetic transaminase, and lysosomal enzymes (Katzman and Wilson, 1974). These cells also became... 

Rutter, G., and Mannweiler, R., 1977, Alterations of actin containing structures in BHK-21 cells infected with Newcastle disease virus and vesicular stomatitis virus, J. Gen. Virol. 37 233. 

Ensminger, W. D., and Tamm, I., 1970, Inhibition of synchronized cellular deoxyribonucleic acid synthesis during Newcastle disease virus, mengovirus or reovirus infection, J. Virol. 5 672. 

Thacore, H. R., and Youngner, J. S., 1971, Cells persistently infected with Newcastle disease virus. III. Chemical stability of hemagglutinin and neuraminidase of a mutant isolated from persistently infected L cells, J. Virol. 1 53-58. 

The ability of the virus to agglutinate erythrocytes has been first reported in 1941. It took more than a decade before it was shown that influenza virus binds to erythrocytes and other cells via 7 -acetylneuraminic acid residues present on the cell surface and that this binding is a prerequisite for initiation of infection [24,25]. Other viruses, such as Sendai, Newcastle disease, polyoma and rotavirus also exhibit an affinity for sialie... 

Significant antiviral ejfectivity was shown in vitro for titanocene dichloride (I) against numerous DNA and RNA viruses in the extracellular phase Typical examples of viruses, which were inhibited by direct contact with I and lost infectivity up to 100%, were orthopoxvirus (vaccinia) and herpes virus (pseudorabies) as DNA viruses, and rhabdovirus (vesicular stomatitis), paramyxovirus (Newcastle disease) and diverse orthomyxoviruses (e.g. influenza A and B) as RNA viruses. A comparable antiviral effect against herpes viruses was detectable after application of the ferricenium salt whereas, on the other hand, vanadocene dichloride (11) and molybdenocene dichloride (V) failed to show antiviral activity under the same experimental conditions. 

Kethoxal, 3-ethoxy-2-oxobutanal hydrate [CH3. CH(OEt).CO.CH-(OH) ] was the first substance, selectively, to inactivate complete virions, namely those causing Newcastle bird disease and influenza tested in embryonated eggs (Tiffany et al, 1957). 2-Thiouracil 12,44) a potent inhibitor of the reproduction of plant viruses, also decreases the infectivity of poliovirus by reaction with a mercapto-group in the capsid (Steele and Black, 1967). However agents such as these which act on the complete virion have not yet proved clinically successful. 

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