Indirect method for prediction of hemagglutination inhibition antibody titers to Newcastle disease virus in chickens by titration of antibodies in egg yolk.
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Attempts were made to establish methods for indirect prediction of hemagglutination inhibition (HI) antibody titers to Newcastle disease virus (NDV) in sera of laying hens and day-old chicks by determining if these are correlated to HI titers in egg yolks. For this purpose, geometric means of HI antibody titers in sera from 60 hens, yolks from 60 matched eggs, and sera from 180 day-old chicks of an identical vaccination program were measured and plotted. There was a significant correlation between HI antibody titers in yolks (X) and hens (Y), with a linear regression of Y = 23.24 + 0.47X and a correlation coefficient of r = 0.65. The linear regression between HI antibody titers in yolks (X) and chicks (Y) was Y = 6.33 + 0.36X (r = 0.58). Immunity to NDV in hens and their offspring can be maintained effectively, and the proper time for the vaccination or booster can be determined by reference to HI titers predicted from the linear regression in the present study. The approach of testing egg yolk for HI titers provides a feasible alternative to determining HI titers from blood samples and eliminates stress in birds during blood sampling. (+info)
Newcastle disease virus nucleocapsid protein: self-assembly and length-determination domains.
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The nucleocapsid protein (NP) of Newcastle disease virus expressed in E. coli assembled as ring- and herringbone-like particles. In order to identify the contiguous NP sequence essential for assembly of these particles, 11 N- or C-terminally deleted NP mutants were constructed and their ability to self-assemble was tested. The results indicate that a large part of the NP N-terminal end, encompassing amino acids 1 to 375, is required for proper folding to form a herringbone-like structure. In contrast, the C-terminal end covering amino acids 376 to 489 was dispensable for the formation of herringbone-like particles. A region located between amino acids 375 to 439 may play a role in regulating the length of the herringbone-like particles. Mutants with amino acid deletions further from the C-terminal end (84, 98, 109 and 114 amino acids) tended to form longer particles compared to mutants with shorter deletions (25 and 49 amino acids). (+info)
Effect of multiplicity of infection on Newcastle disease virus-HeLa cell interaction.
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The effects of a hundred-fold difference in virus/cell multiplicity on the interaction of Newcastle disease virus (NDV) with HeLa cells were studied, and various phases of the virus reproductive cycle were related to cellular consequences of infection. At both multiplicities used all cells were infected. The following events occurred 1 to 2 hours earlier in cells which were inoculated with the higher multiplicity: (a) first appearance of newly made virus antigen, and the amount present at any time during the period of rapid increase; (b) onset and time course of production of infective virus; (c) development by infected cells of hemadsorbing ability; (d) onset and time course of inhibition of mitosis; and (e) onset and time course of marked cell damage. Double infection of HeLa cells with NDV and NWS was demonstrated by the fluorescent antibody technique, and was used to show that the establishment of interference against NWS was also dependent upon the multiplicity of NDV. In cells inoculated at each multiplicity, newly made virus antigen appeared at the same time as the first infective virus particles. Infective virus rapidly reached a peak, and then declined. Viral antigen continued to increase for several hours after the decline in infective virus had begun. Thus, only a small fraction of the virus antigen produced was incorporated into new infective particles. The maximal yield of such particles was only 6 to 11 per HeLa cell. Over 95 per cent of new virus was cell-associated, but could be neutralized by treatment with antiserum before disruption of cells. Mitosis occurred in cells which had produced and released infective NDV. Progressive inhibition of mitotic activity in infected cells was correlated with continued production of viral antigen. Marked cytopathic changes developed after mitotic activity had decreased to low levels. The mechanism by which NDV inhibits mitosis in HeLa cells is discussed. (+info)
Enumeration of cell-infecting particles of Newcastle disease virus by the fluorescent antibody technique.
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A procedure has been developed for the determination of the concentration of infective Newcastle disease virus (NDV) based on the enumeration of singly infected and distributed HeLa cells which are visualized by staining with fluorescent antibody. Infective virus assayed by the fluorescent cell-counting procedure is expressed in terms of cell-infecting units (CIU). Adsorption of NDV to HeLa cell monolayers reached a plateau 1 to 1.5 hours after inoculation of coverslip cultures, and 12 per cent of the infective particles inoculated failed to adsorb. The half-life of NDV in protein-free Eagle's medium at 37 degrees C. was 2.1 hours. There was a linear relationship between virus concentration and the number of infected cells. The coefficient of variation of the mean of replicate determinations of infective NDV was 8.2 per cent. The distribution of single infected HeLa cells in the monolayer corresponded to the Poisson distribution. With NDV the cell-infecting unit (CIU) determined in HeLa cells is equivalent to the plaque-forming unit in chick embryo cells and the egg infective dose. In experiments on the mechanism of dissemination of NDV in monolayer cultures of HeLa cells, NDV was found to spread from cell to cell through the extracellular milieu. (+info)
The pathogenesis of infection with a virulent (CG 179) and an avirulent (B) strain of Newcastle disease virus in the chicken. I. Comparative rates of viral multiplication.
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The comparative growth rates of a virulent (CG 179) and an avirulent (B) strain of NDV in the chicken were analyzed. Following intramuscular inoculation, the CG 179 and B strains both increased at the same rate in the extraneural tissues, i.e. the blood, lung, rectum, and spleen, but the CG 179 strain showed an accelerated growth rate in the brain. The CG 179 strain also multiplied more rapidly in the brain than the B strain following intracerebral administration of minimal inocula. Recovery with the B strain was associated with a decline in virus titer, first in the circulating blood, then in the visceral organs, and lastly in the central nervous system. Certain neuropathological observations were correlated with the pattern of virus growth. (+info)
The pathogenesis of infection with a virulent (CG 179) and an avirulent (B) strain of Newcastle disease virus in the chicken. II. Development of antibody.
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Circulating antibody appeared in the convalescing NDV-infected chicken concomitantly with the disappearance of virus from the tissues. The antigenic response to the CG 179 and B strains was demonstrated to be approximately equal. The neutralization test in the embryo and the hemagglutination inhibition technique yielded parallel results in the measurement of antibody early in convalescence, but late in convalescence the hemagglutination inhibition titers were relatively lower. This disparity indicates the possible duality of the antibodies. There was a wide ratio between the neutralizing antibody titers found in the brain and in the serum after an asymptomatic infection with NDV. The antibody level in the brain appeared to be related to the extent of virus growth and damage in the central nervous system. It appeared likely that a major factor in determining the virulence of the CG 179 strain was the more rapid attainment in the central nervous system of high virus concentration which outstripped the defense mechanisms of the host. (+info)
Mechanism of production of pulmonary lesions in mice by Newcastle disease virus (NDV).
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Infectious NDV particles produce extensive pulmonary consolidation in the mouse in the absence of demonstrable virus multiplication. The lesions are indistinguishable from those of influenza A virus infection. This effect of NDV was blocked by intranasal injection of RDE or immune serum before virus inoculation, but not by immune serum injected 5 minutes or more after NDV. Influenza A virus infection did not diminish fixation of NDV in excised lungs but did interfere with the injurious action of this agent in the living mouse. The analogy between these reactions and those which take place in a progressive virus infection is pointed out, and the mechanism of production of lesions in virus pneumonias discussed. (+info)
A mucoprotein derived from human urine which reacts with influenza, mumps, and Newcastle disease viruses.
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A mucoprotein, present in normal human urine, has been isolated and obtained in a state of a high degree of purity. A number of the biological, chemical, and physicochemical properties of the substance have been studied. From the results obtained in the present investigation and those reported in succeeding papers (34, 35) it appears that the mucoprotein has a high molecular weight, i.e., of the order of 7.0 x 10(6), consists of thread-like molecules which have axial ratios of approximately 100, and is specifically antigenic. This substance, which appears to be free of contaminating material, possesses in extraordinary degree the capacity to react with influenza, mumps, and Newcastle disease viruses. At equilibrium, with influenza virus, the minimal amount of the substance capable of giving a demonstrable reaction with one hemagglutinating unit of virus appears to be about 0.0003 microg. The mucoprotein is altered by preparations of influenza viruses and its capacity to react with these agents or others is lost. The kinetics of the inactivation process brought about by influenza viruses is in accord with those of well known enzyme-substrate systems. With the exception of the capacity to react with viruses, altered mucoprotein did not differ from the native substance relative to any of the properties examined in the present study. That certain physicochemical properties of the altered mucoprotein are different from those of the native substance is demonstrated in succeeding papers (34, 35). (+info)