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Natural infection of broiler breeder chickens with endemic apathogenic Newcastle disease virus and their subsequent response to vaccination with a live V4 Newcastle disease virus vaccine.

Flocks of broiler breeder chickens housed on a commercial farm were monitored from 13 w of age for natural infection with endemic lentogenic Newcastle disease virus (NDV). Seroconversion was first detected at 17 w. By 24 w, all 8 flocks had achieved peak log2 mean haemagglutination inhibiting antibody titres of up to 4.8. Antibody titres then declined and rose again over several months, suggesting cyclic reinfection with NDV. A lentogenic NDV indistinguishable from V4 was isolated from the cloaca of one bird at 18 weeks of age. At 54 weeks of age, 6 of 8 flocks were vaccinated en masse with live V4 NDV vaccine, 3 flocks by drinking water and 3 flocks by aerosol. All flocks were serologically monitored for a further 8 w. Drinking water vaccination induced an anamnestic response in 3 flocks, showing that flocks with pre-existing active immunity to NDV may be successfully vaccinated with V4. However, in all aerosol vaccinated flocks, the procedures failed to induce a response different to that observed in unvaccinated flocks. The serological response to vaccination was greater in sires than in dams.

Animals↗

Quantitative measurement of paramyxovirus fusion: differences in requirements of glycoproteins between simian virus 5 and human parainfluenza virus 3 or Newcastle disease virus.

To compare the requirements for paramyxovirus-mediated cell fusion, the fusion (F) and hemagglutinin-neuraminidase (HN) glycoproteins of simian virus 5 (SV5), human parainfluenza virus 3 (HPIV-3), and Newcastle disease virus (NDV) were expressed individually or coexpressed in either homologous or heterologous combinations in CV-1 or HeLa-T4 cells, using the vaccinia virus-T7 polymerase transient expression system. The contribution of individual glycoproteins in virus-induced membrane fusion was examined by using a quantitative assay for lipid mixing based on the relief of self-quenching (dequenching) of fluorescence of the lipid probe octadecyl rhodamine (R18) and a quantitative assay for content mixing based on the cytoplasmic activation of a reporter gene, beta-galactosidase. In these assays, expression of the individual F glycoproteins did not induce significant levels of cell fusion and no cell fusion was observed in experiments when cells individually expressing homologous F or HN proteins were mixed. However, coexpression of homologous F and HN glycoproteins resulted in extensive cell fusion. The kinetics of fusion were found to be very similar for all three paramyxoviruses studied. With NDV and HPIV-3, no cell fusion was detected when F proteins were coexpressed with heterologous HN proteins or influenza virus hemagglutinin (HA). In contrast, SV5 F protein exhibited a considerable degree of fusion activity when coexpressed with either NDV or HPIV-3 HN or with influenza virus HA, although the kinetics of fusion were two- to threefold higher when the homologous SV5 F and HN proteins were coexpressed. Thus, these data indicate that among the paramyxoviruses tested, SV5 has different requirements for cell fusion.

Animals↗

Transmissibility of Australian strains of Newcastle disease virus.

The transmission of Newcastle disease virus strains from infected to direct-, indirect-, and aerosol-contact groups of chickens was studied. Chickens 7, 21, and 63 days old were used in separate trials. Chicken age and virus strain were found to be important in spread of the virus. Strain V4 spread quickly to all contact groups and was classed as highly transmissible, whereas strain JA failed to infect all contact chickens of each age group, thus spreading less efficiently than strain V4. The viruses spread more readily among the 2 older groups. The significance of the transmissibility of Newcastle disease virus vaccine is briefly discussed.

Age Factors↗

The isolation of lentogenic strains of Newcastle disease virus in Australia.

Twelve isolations of Newcastle disease virus were made from 77 clinical samples from chickens from conjunctivitis, respiratory disease, proventriculitis and bursal atrophy. Nine of the isolations were made from chickens with conjunctivitis. The viruses were identified as Newcastle disease virus by inhibition of their haemagglutinins with specific antiserum to Newcastle disease virus. The viruses failed to kill chicken embryos after inoculation into the allantoic cavity and they were judged to be lentogenic strains. There was no evidence that the Newcastle disease viruses were responsible for any of the clinical conditions from which they were isolated. The presence of other agents in 10 of the samples was indicated by reduced production of haemagglutinin in allantoic fluids of infected embryos, by deaths of infected embryos, by the production of cytopathic changes in avian cell cultures and by electron microscopy. Three isolations of infectious bronchitis virus, 2 of avian adenovirus and one of avian reovirus were made. Other samples were suspected of containing infectious bronchitis virus and mycoplasmas, but these were not isolated. The Newcastle disease viruses failed to produce plaques in chicken embryo fibroblast cell cultures and they were separated from the contaminating agents by haemagglutination and elution followed by passage at terminal dilution in chick embryos. No Newcastle disease virus was isolated from 60 caecal tonsils and 60 lung samples from 9-week-old broiler chickens. Eight lung samples yielded mycoplasmas that caused haemadsorption in chicken cell cultures. The mycoplasmas were probably Mycoplasma gallisepticum.

Animals↗

A case of human infection with Newcastle disease virus.

A case of Newcastle disease virus infection in a female laboratory technician is reported for the first time in Malaysia. Infection was acquired by droplet infection of the eye while grinding infected chicken in the laboratory. The case was confirmed by isolation of Newcastle disease virus from an eye swab taken from the subject on the first day of clinical signs. A four-fold rise of haemagglutination-inhibition titre was shown when sera on the third day of infection and 15 days later were compared.

Adult↗

Antibody detection in matched chicken sera and egg-yolk samples by commercial enzyme-linked immunosorbent assay kits for Newcastle disease virus, infectious bronchitis virus, infectious bursal disease virus, and avian reovirus.

ELISA kits have been used to detect antibody in egg yolk. The major advantage eggs offer over blood samples is the ability to collect samples without compromising flock biosecurity. A disadvantage to using egg yolk over sera concerns the method of preparing yolk for antibody testing. The technique used in this study involved a simple dilution method with no mixing or extraction. To determine the adequacy of yolk samples to replace serum samples, a serum sample and the first six eggs were obtained from each of 50 commercial leghorn hens. Mean titers were consistently larger for serum than for yolk, but the size of the difference varied with the virus. The variation of mean egg titer was comparable to that of the serum titer. Correlations between a hen's serum titer and the mean titer from hen eggs were only moderate, ranging from 0.35 to 0.85 across viruses and systems. The ability to predict the serum titer of a single hen by the mean titer from hen eggs may be inadequate.

Animals↗

Multivalent inactivated virus oil emulsion vaccines in broiler breeder chickens. I. Newcastle disease virus and infectious bursal disease virus bivalent vaccines.

Inactivated Newcastle disease virus (NDV) and infectious bursal disease virus (IBDV) were incorporated into water-in-oil emulsion vaccines alone or as a bivalent vaccine. Twenty-week-old broiler breeder chickens that had received previous live virus vaccination with NDV and IBDV were injected intramuscularly with the monovalent or bivalent vaccine. The antibody titers to either the monovalent vaccine or bivalent vaccine increased rapidly and then remained at high levels for the duration of the 40-week trial. There were no practical differences in amplitude or duration of the antibody response to either antigen used alone compared to that of the bivalent combination. Progeny hatched from the vaccinated breeders possessed maternal antibody levels at one day of age comparable to those of the hens at the time the eggs were laid. The maternal antibody titers declined at a steady rate until they reached negligibly detectable levels at approximately 3 weeks of age. This trend held true without regard to the initial antibody titer.

Animals↗

In ovo interference of embryo non-lethal avian infectious bronchitis viruses (IBV) with velogenic Newcastle disease virus and embryo adapted IBV.

Avian infectious bronchitis virus (IBV) interfered with the lethal effects of velogenic Newcastle disease virus (NDV) and embryo adapted IBV in eggs previously inoculated with non-lethal IBV. Greater interference was noted in eggs superinfected with embryo adapted IBV than velogenic NDV. The interference could be eliminated by treating the initial IBV with homologous anti-IBV serum.

Animals↗

Duration of excretion of virulent Newcastle disease virus following challenge of chickens with different titres of serum antibody to the virus.

Virulent Newcastle disease virus (NDV) was isolated from susceptible and immune chickens following intra-ocular challenge with the Essex '70 strain. Challenge virus was isolated from the trachea and cloaca of susceptible birds until they died 7 to 9 days after challenge. This virus was isolated from immunised chickens for up to 14 days after challenge. The duration of excretion was influenced by the prechallenge serum antibody titre to NDV. It persisted longest in chickens with titres of 2(3) to 2(7) and decreased in length and frequency from chickens with titres in the range 2(8) to 2(12). Chickens with pre-challenge titres of 2(3) to 2(5) developed 2- to 3- fold increases in post-challenge titres, whereas those with higher pre-challenge titres had smaller proportional increases in titre. Excretion of virulent virus from immunised birds should be considered in the development of Newcastle disease control programs.

Animals↗

Phylogenetic analysis of Newcastle disease virus in Taiwan.

The virulent forms of Newcastle disease virus cause a devastating disease of poultry. Between 1998 and 2000, sporadic outbreaks of Newcastle disease occurred in Taiwan despite vaccination. The causes of the failure of the vaccination remain unclear. The purpose of this study was to investigate the possible factors causing these outbreaks by serologic and virologic methods. Anti-Newcastle disease virus hemagglutination-inhibition titers were measured for serum samples obtained from a breeder farm and a broiler farm. The serologic data showed continued presence of virulent Newcastle disease viruses in the field during inter-outbreak periods. Phylogenetic analysis demonstrated that the field virulent Newcastle disease viruses were genetically similar and were grouped into genotype VIIa. Efficacy testing by virulent Newcastle disease virus challenge revealed that the vaccines used were effective for protecting chickens from infections. This investigation demonstrated that the Newcastle disease virus strain can spread quickly and widely throughout a large geographic area, and that the sporadic cases originate from virulent Newcastle disease viruses present in the field.

Animals↗

[Utilization of poly U-cellulose and poly U-sepharose for the study of virus-specific RNA of Newcastle disease virus].

Comparative characteristics of poly(U)-cellulose and poly(U)-sepharose used for the study of virus-specific 18S RNA of Newcastle disease virus are presented. Upon chromatography of 18S NDV RNA on any of these columns, approximately 60-70% RNA was adsorbed. The sorbing RNA contained in poly(A) 10-12% of the total amount of adenosine, in contrast to RNA not adsorbed on the column in which poly(A) contained 1-2% of the total amount of adenosine in RNA molecule. The analysis in sucrose density gradient and polyacryl amide gel of the RNAs eluated from the columns showed RNA chromatography under the conditions used not to cause its degradation. The advantages and short-comings of the sorbents used in studies of virus-specific RNA are discussed.

Cellulose↗

The effect of delayed harvesting as well as freezing and thawing on biological properties of Newcastle disease virus.

Delayed harvest of Newcastle disease virus (NDV) from eggs was less infective (as expressed by its lower infectious titer and a higher number of virus particles per EID50) and more resistant to a temperature of 50 degrees C than the early harvest. On the other hand, little or no effect of delayed harvesting was found on neuraminidase, erythrocyte-fusing and immunogenic properties. Moreover, haemolytic activity of NDV was moderately enhanced when its harvesting from de-embryonated egg was delayed. Treatment of a fresh NDV preparation with repeated freezing and thawing cycles also caused a marked reduction in virus infectivity and induction of its haemolytic activity.

Animals↗

Intracellular processing of the vesicular stomatitis virus glycoprotein and the Newcastle disease virus hemagglutinin-neuraminidase glycoprotein.

The kinetics of intracellular transport of the vesicular stomatitis virus (VSV) glycoprotein (G) and the Newcastle disease virus (NDV) hemagglutinin-neuraminidase (HN) glycoprotein in chicken embryo cells were compared. To assay for the appearance of pulse-labelled glycoprotein at the cell surface, an antibody-binding assay was developed which allowed the precipitation of only those molecules on the outside surfaces of infected cells. Using this assay, it was found that pulse-labelled VSV G protein appeared at the cell surface with a half-time of approximately 27 min, while pulse-labelled NDV HN glycoprotein reached the cell surface with a half-time of approximately 78 min. To determine the transit time of these glycoproteins to trans-Golgi membranes, the kinetics of the acquisition of endoglycosidase H resistance was analyzed. The half-time of the transit of the G protein to the trans-Golgi membranes was found to be approximately 13 min while that of the HN glycoprotein was found to be approximately 60 min. Since the G protein migrates to the trans-Golgi membranes with a half-time of 13 min, and the cell surface with a half-time of 27 min, the half-time for the transit between the trans-Golgi membrane and the plasma membrane must be approximately 14 min. In a similar analysis, the half-time for the transit of the HN glycoprotein from the trans-Golgi membrane to the plasma membrane must be approximately 18 min, a time not significantly different from that of the G protein. Thus the difference in the kinetics of the intracellular transport of these two glycoproteins resides primarily in the transit from the rough endoplasmic reticulum to the trans-Golgi membranes. These results argue against a non-selective mechanism for the transport of plasma membrane glycoproteins to the cell surface.

Animals↗