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Relationship of common avian pathogen antibody titers in so-called chicken anemia agent (CAA)-antibody-positive chicks to titers in CAA-antibody-negative chicks.

Antibody titers for infectious bursal disease virus (IBDV), infectious bronchitis virus, Newcastle disease virus, and reovirus from chicks with chicken anemia agent (CAA) antibodies were compared with antibody titers from their CAA-antibody-negative counterparts. These comparisons were made in 396 chickens that were 1 day, 2 weeks, 8-9 weeks, 10 weeks, 17 weeks, or 29-32 weeks old. Only one serum sample was collected from any given chick or chicken. There were no significant differences between the antibody titers at any age for any antigen, with one exception: at 29-32 weeks, the IBDV titers were higher (t = 2.62, df = 142, P less than 0.01) in chickens with CAA antibody. Although not at all likely, we believe that the observation of high IBDV antibody titers in CAA-antibody-positive chicks could have been a spurious one.

Anemia↗

The propagation of avian viruses in a continuous cell line (QT35) of Japanese quail origin.

Seven of nine avian virus families tested (Birnaviridae, Coronaviridae, Herpesviridae, Paramyxoviridae, Poxviridae, Reoviridae, and Retroviridae) were found to replicate in a quail fibroblast cell line, designated QT35, resulting in a cytopathic effect (CPE) visible with the naked eye or by low-power microscopy. In comparison, only one (Paramyxoviridae) of seven mammalian virus families tested produced an observable CPE. Cytopathic changes induced by examined viruses were round cell, syncytial, and focus formation. Trypsin did not promote cytopathic changes by selected CPE-negative avian and mammalian viruses in QT35 cells. Several avian viruses (infectious bursal disease virus, Newcastle disease virus, Canary pox virus, and reovirus) formed plaques under agar. Avian reovirus and infectious bursal disease virus produced similar titers in chicken embryo fibroblast (CEF) and QT35 cell cultures. Chicken-egg-yolk neutralizing-antibody titers to IBDV were comparable in CEF and QT35 cell-culture systems.

Animals↗

[Serologic monitoring of pullet and laying hen flocks in Switzerland: results from the years 1990 and 1991].

In 1990 and 1991 4522 blood samples from 398 pullet flocks and 1338 blood samples from 128 laying flocks were monitored for antibody against infectious bronchitis virus, infectious laryngotracheitis virus, adenovirus, reovirus, infectious bursal disease virus, Newcastle disease virus, Mycoplasma gallisepticum and Mycoplasma synoviae. The results are discussed for pullets and laying hens.

Animals↗

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.

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.

Animals↗

Genetic stability of Newcastle disease virus CG179: a strain containing only clear plaque subpopulations.

Two cultures of the CG179 strain of Newcastle disease virus were maintained apart in two laboratories for over 30 years. One culture had been passaged 45 times through embryonated chicken eggs, yet this virus had the same virulence, thermostability of hemagglutinin, plaque types, and RNA fingerprint as a culture lyophilized in 1948. The genetic stability observed here has not been reported for strains containing both red and clear plaques and may occur only in strains like CG179 that do not have red plaques.

Animals↗

Serological response of chickens, turkeys and ducks to strain V4 of Newcastle disease virus.

The serological response of two different age groups of turkeys and ducks to strain V4 of Newcastle disease virus was markedly inferior to that of similar age groups of chickens. This suggested that this strain might not be a suitable vaccine strain for use in turkeys and ducks, even though the correlation between specific serum antibody and immunity in these species is not clearly understood. The 20-week-old group of chickens required two doses of 10(7.1) 50 per cent embryo infective doses (EID50) of the virus to develop a specific serum antibody titre comparable to 21-day-old chickens given one dose of 10(7.1) EID50 of virus.

Age Factors↗

Rapid pathotyping of Newcastle disease virus using a single-chain Fv displayed on phage against the C-terminal end of the F2 polypeptide.

Filamentous bacteriophage display technology has been used to generate specific antibody fragments for differentiating virulent and avirulent Newcastle disease virus. A single-chain Fv fragment to the motif (112)RRQ(114), present at the F2 C-terminal end of many virulent Newcastle disease virus isolates, was isolated from a phage display library derived from a rabbit immunized with a peptide conjugate. An ELISA evaluation was carried out to test its ability to differentiate between 11 avirulent and 34 virulent NDV isolates. The antibody fragment reacted with 25/28 virulent viruses with the putative motif (112)RRQ(114). The three exceptions were viruses with an arginine instead of glycine, at position 110 of the fusion protein, just preceding the cleavage site. Five of six virulent isolates, whose predicted motif was different from that usually found in virulent strains, also tested negative. However, the antibody did react with one isolate with the motif (112)KRQ(114). There was no apparent reactivity with any of the avirulent isolates tested. We conclude that this antibody may, in the future, be a useful aid for the pathotyping of NDV isolates.

Amino Acid Motifs↗

Electrocardiographic and respiratory responses to viscerotropic and neurotropic strains of Newcastle disease virus measured by radio telemetry.

Two groups each of White Rock chickens from 6 to 23 weeks old were monitored by radio telemetry to determine their electrocardiogram and respiration response after they were infected with either a velogenic viscerotropic isolate of Newcastle disease virus (VVND) or the neurotropic GB strain of Newcastle disease virus (NGB). Significant changes were found in the heart rate, R wave amplitude, ST segment elevation, T wave amplitude, RS complex interval, ST segment duration T wave interval, TP segment duration, PR segment duration and TP interval of the birds infected with VVND, but no significant ECG changes were found in the birds infected with NGB. There were no significant changes in respiration rate in any birds.

Animals↗

Selection of temperature-sensitive mutants during persistent infection: role in maintenance of persistent Newcastle disease virus infections of L cells.

Virus mutants (NDV(pi)) recovered from L cells persistently infected with Newcastle disease virus (NDV, Herts strain) are temperature-sensitive (ts) at 43 C, although the wild-type virus (NDV(o)) which initiated the persistent infection replicates normally at that temperature. To study the relationship between the ts marker of NDV(pi) and the other properties which distinguish this virus from NDV(o), NDV(pi) ts(+) revertants were selected at the nonpermissive temperature and NDV(o) ts mutants were generated by treating NDV(o) with nitrous acid. Spontaneously-occurring ts mutants in the Herts NDV population were also isolated. The different virus populations were characterized with regard to plaque size, virulence for eggs, and thermal stability of infectivity, hemagglutinin, and neuraminidase. The NDV(pi) ts(+) revertants, although no longer temperature-sensitive, retained NDV(pi) properties, whereas both spontaneously-occurring and mutagen-induced ts mutants remained wild-type in their other properties. These findings showed that the properties which characterized NDV(pi) were independent of the ts marker. However, the ts marker and the other markers of NDV(pi) were coselected during the persistent infection, and the combination of those markers appeared to be important in the outcome of NDV infection of L cells. NDV(pi) replicated productively in L cells, whereas NDV(o), the NDV(pi) ts(+) revertants, and the spontaneously-occurring ts mutants all yielded covert infections in L cells. The role of the selection of ts mutants in persistent infection was confirmed as follows: L cells were persistently infected with NDV(pi) ts(+) revertants and NDV(o) ts mutants. Virus recovered from the persistently infected cultures after eight cell passages was always temperature-sensitive and of smaller plaque size than the parental virus in chicken embryo cell cultures. Similar results were obtained with virus recovered from L-cell cultures persistently infected with two other velogenic strains of NDV, the Texas-GB and Kansas-Man strains. These results strongly suggest that selection of ts mutants during the persistent infection was not random and played a role in establishment or maintenance of the persistent infection, or both.

Animals↗

[Newcastle disease virus in tissue cultures studied by an immunofluorescence method].

Studied was the opportunity to demonstrate the Newcastle Disease Virus in tissue cultures with the employment of an immunofluorescence method. The development was followed up of four strains--the vaccinal ones Hitchner B1, La Sota, and Komarov and the velogenic one, Texas GB, using chick fibroblasts. It was found that the velogenic strain cumulated earlier and more intensely than the vaccinal ones, where the virus was seen to explicitly locate perivascularly. The most dependable demonstration of the virus proved possible with the velogenic strain at the 4th hour, and with the vaccinal strains--from the 6 th to the 10 th hour following the infection of the cultures. The virus antigen cumulated progressively, and with the velogenic strain it was accompanied with the production of a cytopathic effect which destroyed the cells by the 20th hour; with the vaccinal strains the cells remained intact up to the 48th hour following infection.

Animals↗

The properdin system and immunity. VI. The inactivation of Newcastle disease virus by the properdin system.

Detailed experiments are presented which indicate that the properdin system is an inhibitor of Newcastle disease virus. Viral inhibition required all known components of the properdin system: properdin, all four components of complement and magnesium; the removal of any one constituent resulted in a loss of inhibition; the replacement of the constituent restored antiviral effect. The inhibition of virus was temperature-dependent. The process of inhibition by serum resulted in a decrease in the amount of properdin available in the serum without any measurable effect on the components of complement. The prolonged incubation of inactive serum-virus mixtures with cation-exchange resin resulted in the restoration of some, but not all, of the hemagglutinating activity of the virus. The requirements of the properdin system and the implication of these findings were discussed.

Animals↗

Modification of normal cell surface by smooth membrane preparations from BHK-21 cells infected with Newcastle disease virus.

Smooth membrane fractions were prepared from the cytoplasmic extract of BHK-21 cells infected with Newcastle disease virus (NDV). These membranes exhibited high hemagglutinating, neuraminidase, and hemolytic activity but little infectivity, suggesting that they might be precursors for viral envelope. When such membranes were adsorbed to the monolayers of uninfected BHK-21 cells at 4 degrees C and then incubated at elevated temperature for a couple of hours, the cells became highly hemadsorptive even in the presence of cycloheximide. This phenomenon occurred between 15 degrees C and 25 degrees C, and was maximal at 31 degrees C, where approximately 4 times more erythrocytes were adsorbed than to the cells incubated at 4 degrees C. Immunofluorescent staining suggested that diffusion of viral antigens might occurred rapidly over the entire surface of the cells. Cell fractions containing virions induced hemadsorption in uninfected cells, too. However, induction occurred now at 31 degrees C and was maximal at 37 degrees C, and erythrocytes appeared to be adsorbed not to the entire surface of the monolayer but restricted areas of the cells. The diffusion of viral antigens on the cell surface was not so significant under these conditions. On the basis of these findings the possible role of the membranes of the smooth endoplasmic reticulum in virus replication is discussed.

Antigens, Viral↗

Determination of the disulfide bond arrangement of Newcastle disease virus hemagglutinin neuraminidase. Correlation with a beta-sheet propeller structural fold predicted for paramyxoviridae attachment proteins.

Disulfide bonds stabilize the structure and functions of the hemagglutinin neuraminidase attachment glycoprotein (HN) of Newcastle disease virus. Until this study, the disulfide linkages of this HN and structurally similar attachment proteins of other members of the paramyxoviridae family were undefined. To define these linkages, disulfide-linked peptides were produced by peptic digestion of purified HN ectodomains of the Queensland strain of Newcastle disease virus, isolated by reverse phase high performance liquid chromatography, and analyzed by mass spectrometry. Analysis of peptides containing a single disulfide bond revealed Cys(531)-Cys(542) and Cys(172)-Cys(196) linkages and that HN ectodomains dimerize via Cys(123). Another peptide, with a chain containing Cys(186) linked to a chain containing Cys(238), Cys(247), and Cys(251), was cleaved at Met(249) with cyanogen bromide. Subsequent tandem mass spectrometry established Cys(186)-Cys(247) and Cys(238)-Cys(251) linkages. A glycopeptide with a chain containing Cys(344) linked to a chain containing Cys(455), Cys(461), and Cys(465) was treated sequentially with peptide-N-glycosidase F and trypsin. Further treatment of this peptide by one round of manual Edman degradation or tandem mass spectrometry established Cys(344)-Cys(461) and Cys(455)-Cys(465) linkages. These data, establishing the disulfide linkages of all thirteen cysteines of this protein, are consistent with published predictions that the paramyxoviridae HN forms a beta-propeller structural fold.

Amidohydrolases↗

Thermostability of the hemagglutinin of Newcastle disease virus as a strain marker in epizootiologic studies.

The recent isolation of viscerotropic velogenic strains of Newcastle disease virus having a thermosensitive hemagglutinin and of a lentogenic strain with an unusually thermostable hemagglutinin confirmed that virulence for chickens was not related to the thermostability and could be used as a marker for strains in epizootiologic investigations.

Hemagglutination Tests↗

Effect of subclinical lead toxicity on the immune response of chickens to Newcastle disease virus vaccine.

The effect of lead acetate (20 and 40 mg kg-1 bodyweight daily) administered via the crop from day old to 56 days of age on the immune response to Newcastle disease virus vaccine (NDVV, La Sota strain) was studied in 354 Lohman chickens. Lead decreased the mitogenic response of peripheral blood lymphocytes (PBL) to phytohaemagglutinin-P (PHA-P) in birds vaccinated with NDVV. It also decreased the weights of the bursa of Fabricius, the thymus glands and the spleen relative to bodyweight. Lead administration decreased the antibody titre to NDVV in the vaccinated groups. The percentage mortality due to a challenge with a virulent velogenic Newcastle disease virus was higher in the lead intoxicated birds.

Animals↗