“Red Legs” in Australian Chicks

Retnasabapathy, A; Kheng, Chong Sue

doi:10.1111/j.1751-0813.1963.tb04189.x

Cited by 6 publications

(1 citation statement)

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“…In 1963, chickens exported from Australia to Malaysia were reported to be infected with ND, however serosurveys conducted in response to this claim did not find any evidence of the virus in the Australian poultry flock 37,38 . The next detection of ND in Australia was not made until 1966, when a lentogenic strain termed 'V4' was found in broilers in Queensland as part of a mixed infection with other viral and parasitic agents 39 .…”

Section: S: Avirulent Endemic Ndv Strainsmentioning

confidence: 99%

The molecular basis of the pathogenicity of Newcastle disease virus in chickens

Bergfeld¹

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Newcastle disease (ND) is a highly pathogenic disease of poultry and is caused by virulent strains of Newcastle disease virus (NDV). From 1998From -2002 there were outbreaks of ND in Australia which resulted in significant disruptions to the poultry industry. In some of these outbreaks however, the clinical signs observed in the infected birds did not appear to correlate with the World Organisation for Animal Health's definition of a virulent virus, which is based on the molecular sequence at the fusion protein cleavage site. In one particular outbreak at Meredith, Victoria, in 2002, a virulent virus was isolated, despite only a minimal increase in mortalities on the property. Therefore, this thesis has attempted to determine whether, in addition to the fusion protein cleavage site, there are other molecular determinants of pathogenicity for NDV. NDV. Sequence analysis showed a number of amino acid differences throughout the genomes of the four viruses studied, however none of these differences were in key areas such as glycosylation sites. The Meredith/02 virus was also shown to replicate well in embryonated eggs, throughout the chorioallantoic membrane and internal organs of the embryo, including the lung, liver and kidneys. This is consistent with other virulent NDVs.ii The V protein of the Meredith/02 virus was investigated for its role in potential attenuation of the virus via modulation of the host innate immune response. However there was no difference found in the ability of the Meredith/02 V protein to antagonise type I interferon in-vitro when compared with the Herts 33/56 virus.In an attempt to analyse the viral replication complex, to identify a specific protein that may be involved with the minimal pathogenicity of the Meredith/02 virus, the transcription gradient of the virus was characterized. It was found that the Meredith/02 virus has an increased transcription gradient when compared with the Herts 33/56 virus. The gradient of the Meredith/02 virus was particularly steep at the N-P junction, with particularly low levels of the P gene transcribed at 24 hours. However, gene start and end sequences at this location did not vary between the two viruses, thereby indicating that the N and P proteins are less likely to be associated with the steepened gradient. Instead, this suggests a possible role for the large polymerase protein in decreasing transcription.Whilst this research has not yet identified specific molecular sequences responsible for the minimal pathogenicity of the Meredith/02 virus despite its virulent fusion protein cleavage site, it has focused the investigation on components of the viral replication complex.Therefore directions for further research include investigating the role of the replication complex, in particular, the large polymerase (L) gene in the pathogenicity of Australian NDVs. This could also incorporate further work on the individual proteins via the use of minigenome assays, or by utilising reverse genetics and full-length virus clones.

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Section: S: Avirulent Endemic Ndv Strainsmentioning

confidence: 99%