Publications

The Pirbright Institute publication directory contains details of selected publications written by our researchers.

There were a total of 2599 results for your search.

Abstract

Slaughter by puntilla followed by neck sticking was examined in 20 recumbent llamas. Repeat stabbing was needed to penetrate the foramen ovale in 45% of the llamas, and two animals attempted to stand after the first stab. Puntilla was found to be ineffective, as all animals showed rhythmic breathing movements at the flank following puntilla and before sticking, and 95% had a positive palpebral reflex at the same time. The findings indicated that it is difficult in practice to penetrate the spinal cord with a single puntilla stab.

Alpar H O, Bramwell V W, Veronesi E, Darpel K E, Pastoret P-P, Mertens P P C (2009)

Bluetongue virus vaccines past and present (Chapter 18)

Bluetongue (edited by P Mertens, M Baylis, P Mellor, Academic Press), 397-428
Publisher’s version:
Darpel K E, Monaghan P, Anthony S J, Takamatsu H-H, Mertens P P C (2009)

BTV in the mammalian host and the induced immune response (Chapter 12)

Bluetongue (edited by P Mertens, M Baylis, P Mellor, Academic Press), 265-284
Publisher’s version:
Ross-Smith N, Darpel K E, Monaghan P, Mertens P P C (2009)

Bluetongue virus: Cell biology (Chapter 5)

Bluetongue (edited by P Mertens, M Baylis, P Mellor, Academic Press), 77-100
Publisher’s version:
Maclachlan N J, Drew C P, Darpel K W, Worwa G (2009)

The pathology and pathogenesis of bluetongue

Journal of Comparative Pathology 141 (1), Jan-16

Abstract

Bluetongue (BT) is an insect-transmitted viral disease of wild and domestic ruminants and, occasionally, other species. Amongst domestic livestock, BT is most common in certain breeds of sheep whereas asymptomatic BT virus (BTV) infection of cattle is typical in enzootic regions. BT in cattle can be a feature of specific outbreaks, notably the current epizootic in Europe caused by BTV serotype 8. BTV replicates within mononuclear phagocytic and endothelial cells, lymphocytes and possibly other cell types in lymphoid tissues, the lungs, skin and other tissues. Infected ruminants may exhibit a prolonged but not persistent viraemia and BTV is associated with erythrocytes during the late stages of this prolonged viraemia. The pathogenesis of BT involves injury to small blood vessels in target tissues, but the relative contributions of direct virus-induced cytolysis and virus-induced vasoactive mediators in causing endothelial injury and dysfunction are presently unclear. The lesions of BT are characteristic and include: haemorrhage and ulcers in the oral cavity and upper gastrointestinal tract; necrosis of skeletal and cardiac muscle; coronitis; subintimal haemorrhage in the pulmonary artery; oedema of the lungs, ventral subcutis, and fascia of the muscles of the neck and abdominal wall; and pericardial, pleural and abdominal effusions. Transplacental transmission of BTV in ruminants, with subsequent fetal infection, is a property of specific virus strains, especially those propagated in embryonated eggs or cell culture. The outcome of BTV infection of fetal ruminants is age-dependent, with distinctive cavitating lesions of the central nervous system in animals that survive infection in early gestation. Immune competence to BTV arises by mid-gestation, and animals infected in late gestation can be born viraemic and without significant brain malformations.

Abstract

MicroRNAs (miRNAs) are increasingly recognized to play crucial roles in regulation of gene expression in different biological events, including many sporadic forms of cancer. However, despite the involvement of several viruses in inducing cancer, only a limited number of studies have been carried out to examine the miRNA expression signatures in virus-induced neoplasia, particularly in herpesvirus-induced tumours where virus-encoded miRNAs also contribute significantly to the miRNome of the tumour cell. Marek's disease (MD) is a naturally occurring, rapid-onset CD4+ T-cell lymphoma of poultry, induced by the highly contagious Marek's disease virus (MDV). High levels of expression of virus-encoded miRNAs and altered expression of several host-encoded miRNAs were demonstrated in the MDV-transformed lymphoblastoid cell line MSB-1. In order to identify the miRNA expression signature specific to MDV-transformed cells, we examined the global miRNA expression profiles in seven distinct MDV-transformed cell lines by microarray analysis. This study revealed that, in addition to the high levels of MDV-encoded miRNAs, these MD tumour-derived lymphoblastoid cell lines showed altered expression of several host-encoded miRNAs. Comparison of the miRNA expression profiles of these cell lines with the MDV-negative, retrovirus-transformed AVOL-1 cell line showed that miR-150 and miR-223 are downregulated irrespective of the viral aetiology, whereas downregulation of miR-155 was specific for MDV-transformed tumour cells. Thus, increased expression of MDV-encoded miRNAs with specific downregulation of miR-155 can be considered as unique expression signatures for MD tumour cells. Analysis of the functional targets of these miRNAs would contribute to the understanding of the molecular pathways of MD oncogenicity.

Lam D, Dickens D, Reid E B, Loh S H Y, Moisoi N, Martins L M (2009)

MAP4K3 modulates cell death via the post-transcriptional regulation of BH3-only proteins

Proceedings of the National Academy of Sciences 106 (29), 11978-11983

Abstract

Intracellular signal transduction networks involving protein kinases are important modulators of cell survival and cell death in multicellular organisms. Functional compromise of these networks has been linked to aberrant apoptosis in diseases such as cancer. To identify novel kinase regulators of cell death, we conducted an RNAi-based screen to identify modulators of the intrinsic apoptosis pathway. Using this approach, we identified MAP4K3 as a novel apoptosis inducer. Here, we present evidence that this pro-apoptotic kinase orchestrates activation of BAX via the concerted posttranscriptional modulation of PUMA, BAD, and BIM. Additionally, we found decreased levels of this kinase in pancreatic cancer samples, suggesting a tumor suppressor role for MAP4K3 in pancreatic tumorigenesis.
Kaiser P, Howell M M, Fife M, Sadeyen J R, Salmon N, Rothwell L, Young J, Poh T, Stevens M, Smith J, Burt D, Swaggerty C, Kogut M (2009)

Towards the selection of chickens resistant to Salmonella and Campylobacter infections

Bulletin et Mémoires de l'Académie Royale de Médecine de Belgique 164 (1-2), 17-26

Abstract

Resistance to infection with enteric pathogens such as Salmonella and Campylobacter can be at many levels and include both non-immune and immune mechanisms. Immune resistance mechanisms can be specific, at the level of the adaptive immune response, or non-specific, at the level of the innate immune response. Whilst we can extrapolate to some degree in birds from what is known about immune responses to these pathogens in mammals, chickens are not "feathered mice", but have a different repertoire of genes, molecules, cells and organs involved in their immune response compared to mammals. Fundamental work on the chicken's immune response to enteric pathogens is therefore still required. Our studies focus particularly on the innate immune response, as responses of heterophils (the avian neutrophil equivalent) from commercial birds, and macrophages from inbred lines of chickens, correlate with resistance or susceptibility to Salmonella infection with a variety of Salmonella serovars and infection models. We work on two basic resistance mechanisms - resistance to colonization with Salmonella or Campylobacter, and resistance to systemic salmonellosis (or fowl typhoid). To map genes involved in resistance to colonization with Salmonella and Campylobacter, we are using a combination of expression quantitative trait loci (eQTLs) from microarray studies, allied with whole genome SNP arrays (WGA), a candidate gene approach and analysis of copy number variation across the genome. For resistance to systemic salmonellosis, we have refined the location ofa novel resistance locus on Chromosome 5, designated SAL1, using high density SNP panels, combined with advanced back-crossing of resistant and susceptible lines. Using a 6th generation backcross mapping population we have confirmed and refined the SAL1 locus to 8-00 kb of Chromosome 5. This region spans 14 genes, including two very striking functional candidates; CD27-binding protein (Siva) and the RAC-alpha serine/threonine protein kinase homologue, AKT1.

Kaiser P, Wu Z, Rothwell L, Fife M, Gibson M, Poh T Y, Shini A, Bryden W, Shini S (2009)

Prospects for understanding immune-endocrine interactions in the chicken

General and Comparative Endocrinology 163 (1-2), 83-91

Abstract

Despite occupying the same habitats as mammals, having similar ranges of body mass and longevity, and facing similar pathogen challenges, birds have a different repertoire of organs, cells, molecules and genes of the immune system when compared to mammals. In other words, birds are not “mice with feathers”, at least not in terms of their immune systems. Here we discuss differences between immune gene repertoires of birds and mammals, particularly those known to play a role in immune-endocrine interactions in mammals. If we are to begin to understand immune-endocrine interactions in the chicken, we need to understand these repertoires and also the biological function of the proteins encoded by these genes. We also discuss developments in our ability to understand the function of dendritic cells in the chicken; the function of these professional antigen-presenting cells is affected by stress in mammals. With regard to the endocrine system, we describe relevant chicken pituitary-adrenal hormones, and review recent findings on the expression of their receptors, as these receptors play a crucial role in modulating immune-endocrine interactions. Finally, we review the (albeit limited) work that has been carried out to understand immune-endocrine interactions in the chicken in the post-genome era.

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