Newcastle Disease Virus (newcastle + disease_virus)

Distribution by Scientific Domains

Selected Abstracts

A serological and virological survey for evidence of infection with Newcastle disease virus in Australian chicken farms

VG Kite
Objective, To determine the prevalence and distribution of antibodies to Newcastle disease virus on Australian chicken farms and to determine the pathotype and relationships of the Newcastle disease viruses present on those farms. Design, A cross-sectional survey of 753 commercial chicken farms. Procedure, The survey comprised a detailed questionnaire and collection of venous blood samples. The titre of antibodies to Newcastle disease virus was determined by haemagglutination inhibition. Virus isolation was conducted from cloacal and tracheal swabs taken from chickens in serologically positive flocks. Virus isolates were pathotyped on the basis of the deduced Fusion protein cleavage site determined by nucleotide sequencing of a 265 bp region of the genome in the region of the cleavage site. Results, Antibody evidence of Newcastle disease virus infection was found on 300 of the 753 surveyed farms throughout all 11 geographic regions of the survey. The highest prevalence occurred in the Sydney basin, New South Wales and Victoria east regions. Antibody titres were also highest in the regions where serologically positive flocks were most prevalent. The 259 virus isolates revealed nine different RNA sequences. Of the nine virus groups isolated, the most common group W was identical in sequence to the V4 vaccine strain. Five of the other groups had novel RNA sequences in the region of the F protein cleavage site. Conclusions, Antibodies to Newcastle disease virus are highly prevalent in the Australian chicken flock but all identified strains were avirulent in nature. [source]

Recombinant newcastle disease virus capsids displaying enterovirus 71 VP1 fragment induce a strong immune response in rabbits

Lalita Ambigai Sivasamugham
Abstract The complete VP1 protein of EV71 was truncated into six segments and fused to the C-terminal ends of full-length nucleocapsid protein (NPfl) and truncated NP (NPt; lacks 20% amino acid residues from its C-terminal end) of newcastle disease virus (NDV). Western blot analysis using anti-VP1 rabbit serum showed that the N-terminal region of the VP1 protein contains a major antigenic region. The recombinant proteins carrying the truncated VP1 protein, VP11,100, were expressed most efficiently in Escherichia coli as determined by Western blot analysis. Electron microscopic analysis of the purified recombinant protein, NPt-VP1,100 revealed that it predominantly self-assembled into intact ring-like structures whereas NPfl-VP1,100 recombinant proteins showed disrupted ring-like formations. Rabbits immunized with the purified NPt-VP1,100 and NPfl-VP1,100 exhibited a strong immune response against the complete VP1 protein. The antisera of these recombinant proteins also reacted positively with authentic enterovirus 71 and the closely related Coxsackievirus A16 when analyzed by an immunofluorescence assay suggesting their potential as immunological reagents for the detection of anti-enterovirus 71 antibodies in serum samples. J. Med. Virol. 78:1096,1104, 2006. © 2006 Wiley-Liss, Inc. [source]

Impaired virus-induced interferon-,2 release in adult asthmatic patients

K. Gehlhar
Summary Background Interferon-, (IFN-,) not only serves as a first defence line of the immune system against viral attacks but also interacts with T-helper type 1 (Th1)/ T-helper type 2 (Th2) regulation and various other cell types like basophils and monocytes, thereby linking innate and acquired immunity. Recently, we demonstrated that children with allergic asthma produced significantly lower amounts of virus-induced IFN-,2 compared with healthy children or those with intrinsic asthma. Objective In this study, we extend our analysis to examine in a cohort study whether IFN-,2 is also reduced in allergic asthma of adults. Methods Adults with allergic asthma and healthy controls were prospectively recruited. Blood cultures were stimulated with different viruses (respiratory syncytial virus (RSV), newcastle disease virus (NDV)) and analysed for IFN-,2 protein release and gene transcription. Results Virus-induced IFN-,2 release from blood cells of allergic asthmatic patients was significantly reduced compared with healthy controls, independent of the virus used (NDVasthma=221±134 pg/mL, NDVhealthy=555±341 pg/mL, P=0.003 and RSVasthma=46±27 pg/mL, RSVhealthy=108±90 pg/mL, P=0.014). Values=mean±standard deviation). It was not influenced by medication, especially cortico-steroids. IFN-,2 mRNA expression 5 h after NDV stimulation confirmed the ELISA results and correlated well with release data (r=0.397, P=0.033). Conclusion Like children, adults with allergic asthma show impaired virus-induced IFN-,2 release in whole blood, indicating a systemic phenomenon in patients with bronchial asthma and atopic phenotype. Impaired virus-induced IFN-, release could be a marker of inflammation in chronic allergic asthma. [source]