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

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Weesendorp E, Morgan S, Stockhofe-Zurwieden N, Popma-De Graaf D J, Graham S P, Rebel J M J (2013)

Comparative analysis of immune responses following experimental infection of pigs with European porcine reproductive and respiratory syndrome virus strains of differing virulence

Veterinary Microbiology 163 (1-2), 1-12
Publisher’s version: http://dx.doi.org/10.1016/j.vetmic.2012.09.013

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) is difficult to control due to a high mutation rate and the emergence of virulent strains. The objective of this study was to analyze the immunological and pathological responses after infection with the European subtype 3 strain Lena in comparison to subtype 1 strains Belgium A and Lelystad-Ter Huurne (LV). Sixteen pigs were inoculated per strain, and sixteen pigs with PBS. At days 7 and 21 post-inoculation (p.i.), four pigs per group were immunized with an Aujeszky disease vaccine (ADV) to study the immune competence after PRRSV infection. Infection with the Lena strain resulted in fever and clinical signs. This was not observed in the Belgium A or LV-infected pigs. Infection with the Lena strain resulted in high virus titers in serum, low numbers of IFN-gamma secreting cells, a change in leukocyte populations and a delayed antibody response to immunization with ADV. Levels of IL-1 beta, IFN-alpha, IL-10, IL-12, TNE-alpha and IFN-gamma mRNA of the Lena-infected pigs were increased during the first week of infection. For pigs infected with the Belgium A or LV strain, the effects of infection on these parameters were less pronounced, although for the Belgium A-infected pigs, the level of the analyzed cytokines, except for TNF-alpha, and leukocyte populations were comparable to the Lena-infected pigs. These results suggest that while the outcome of infection for the three strains was comparable, with mostly clearance of viremia at day 33 p.i, differences in immune responses were observed, perhaps contributing to their virulence.
Wensman J J, Munir M, Thaduri S, Hornaeus K, Rizwan M, Blomstrom A-L, Briese T, Lipkin W I, Berg M (2013)

The X proteins of bornaviruses interfere with type I interferon signalling

Journal of General Virology 94, 263-269
Publisher’s version: http://dx.doi.org/10.1099/vir.0.047175-0

Abstract

Borna disease virus (BDV) is a neurotropic, negative-stranded RNA virus causing persistent infection and progressive neurological disorders in a wide range of warm-blooded animals. The role of the small non-structural X protein in viral pathogenesis is not completely understood. Here we investigated whether the X protein of BDV and avian bornavirus (ABV) interferes with the type I interferon (IFN) system, similar to other non-structural proteins of negative-stranded RNA viruses. In luciferase reporter assays, we found that the X protein of various bornaviruses interfered with the type I IFN system at all checkpoints investigated, in contrast to previously reported findings, resulting in reduced type I IFN secretion.
Willcocks S, Offord V, Seyfert H-M, Coffey T J, Werling D (2013)

Species-specific PAMP recognition by TLR2 and evidence for species-restricted interaction with Dectin-1

Journal of Leukocyte Biology 94 (3), 449-458
Publisher’s version: http://dx.doi.org/10.1189/jlb.0812390

Abstract

TLRs mediate recognition of a wide range of microbial products, including LPS, lipoproteins, flagellin, and bacterial DNA, and signaling through TLRs leads to the production of inflammatory mediators. In addition to TLRs, many other surface receptors have been proposed to participate in innate immunity and microbial recognition, and signaling through some of these, for example, C-type lectins, is likely to cooperate with TLR signaling in defining inflammatory responses. In the present study, we examined the importance of the ECD and intracellular TIR domain of boTLR2 and huTLR2 to induce a species-specific response by creating a chimeric TLR2 protein. Our results indicate that the strength of the response to any TLR2 ligand tested was dependent on the extracellular, solenoid structure, but not the intracellular TIR domain. Furthermore, we examined whether the recognition of two PAMPs by Dectin-1, a CLR, depends on the interaction with TLR2 from the same species. TLR2 expression seemed to affect the Dectin-1-dependent production of CXCL8 to ?-glucan containing zymosan as well as Listeria monocytogenes. Furthermore, the interaction of Dectin-1 with TLR2 seemed to require that both receptors are from the same species. Our data demonstrate that the differences in the TLR2 response seen between the bovine and human system depend on the ECD of TLR2 and that collaborative recognition of distinct microbial components by different classes of innate-immune receptors is crucial in orchestrating inflammatory responses.
Wilson A J, Ribeiro R, Boinas F (2013)

Use of a Bayesian network model to identify factors associated with the presence of the tick Ornithodoros erraticus on pig farms in southern Portugal

Preventive Veterinary Medicine 110 (1), 45-53
Publisher’s version: http://dx.doi.org/10.1016/j.prevetmed.2013.02.006

Abstract

The soft tick Ornithodoros erraticus occurs on pig farms in southern Portugal and Spain and transmits several important pathogens of humans and livestock. Its distribution is patchy and the determinants of its distribution are uncertain. Here, we use a Bayesian network model to explore possible associations between climate, farm management and the presence of O. erraticus. The resulting network confirms previous suggestions that the presence of O. erraticus is more likely in traditionally constructed pig housing, and indicates that carbon dioxide traps are highly effective for the detection of O. erraticus. Our approach also picked up several other intuitively reasonable relationships, including that traditional housing was more likely to be in poor condition and more likely to be out of use, and that buildings which were in use to house pigs were also less likely to be derelict. Neither temperature nor precipitation had any direct effect on the probability of the presence of O. erraticus, suggesting that the distribution of the species is primarily driven by farm management factors.
Xu L, Hurtle W, Rowland J M, Casteran K A, Bucko S M, Grau F R, Valdazo-Gonzalez B, Knowles N J, King D P, Beckham T R, McIntosh M T (2013)

Development of a universal RT-PCR for amplifying and sequencing the leader and capsid-coding region of foot-and-mouth disease virus

Journal of Virological Methods 189 (1), 70-76
Publisher’s version: http://dx.doi.org/10.1016/j.jviromet.2013.01.009

Abstract

Foot-and-mouth disease (FMD) is a highly infectious viral disease of cloven-hoofed animals with debilitating and devastating consequences for livestock industries throughout the world. Key antigenic determinants of the causative agent, FMD virus (FMDV), reside within the surface-exposed proteins of the viral capsid. Therefore, characterization of the sequence that encodes the capsid (P1) is important for tracking the emergence or spread of FMD and for selection and development of new vaccines. Reliable methods to generate sequence for this region are challenging due to the high inter-serotypic variability between different strains of FMDV. This study describes the development and optimization of a novel, robust and universal RT-PCR method that may be used to amplify and sequence a 3 kilobase (kb) fragment encompassing the leader proteinase (L) and capsid-coding portions (P1) of the FMDV genome. This new RT-PCR method was evaluated in two laboratories using RNA extracted from 134 clinical samples collected from different countries and representing a range of topotypes and lineages within each of the seven FMDV serotypes. Sequence analysis assisted in the reiterative design of primers that are suitable for routine sequencing of these RT-PCR fragments. Using this method, sequence analysis was undertaken for 49 FMD viruses collected from outbreaks in the field. This approach provides a robust tool that can be used for rapid antigenic characterization of FMDV and phylogenetic analyses and has utility for inclusion in laboratory response programs as an aid to vaccine matching or selection in the event of FMD outbreaks.
Yamazaki W, Mioulet V, Murray L, Madi M, Haga T, Misawa N, Horii Y, King D P (2013)

Development and evaluation of multiplex RT-LAMP assays for rapid and sensitive detection of foot-and-mouth disease virus

Journal of Virological Methods 192 (1-2), 18-24
Publisher’s version: http://dx.doi.org/10.1016/j.jviromet.2013.03.018

Abstract

This paper describes the evaluation of four novel real-time multiplex reverse transcription loop-mediated isothermal amplification (RT-LAMP) assays for rapid and sensitive diagnosis of foot-and-mouth disease (FMD). In order to overcome the genetic diversity of FMD viruses (FMDV), these multiplex RT-LAMP assay pairs were established by combining four newly designed primer sets with two primer sets that had been previously published. Using a real-time turbidimeter to detect amplification products and a panel of 300 samples collected throughout the world over a 78-year period, the performance of the multiplex RTLAMP assays was compared with a FMDV-specific real-time RT-PCR assay. The most successful of the four multiplex RT-LAMP assays achieved a diagnostic sensitivity and specificity of 98.0% and 98.1%, and did not falsely detect FMDV in known negatives or samples containing swine vesicular disease virus, vesicular stomatitis virus or vesicular exanthema of swine virus. Furthermore, the analytical sensitivity of this multiplex RT-LAMP assay was at least as good as the individual component RT-LAMP tests. This is the first report of the development of a multiplex RT-LAMP to accommodate the high sequence variability encountered in RNA virus genomes and these results support the use of RT-LAMP as a cost-effective tool for simple diagnosis of FMD.
Wright C F, Knowles N J, Di Nardo A, Paton D J, Haydon D T, King D P (2013)

Reconstructing the origin and transmission dynamics of the 1967-68 foot-and-mouth disease epidemic in the United Kingdom

Infection Genetics and Evolution 20, 230-238
Publisher’s version: https://doi.org/10.1016/j.meegid.2013.09.009

Abstract

A large epidemic of foot-and-mouth disease (FMD) occurred in the United Kingdom (UK) over a seven month period in Northwest England from late 1967 to the summer of 1968. This was preceded by a number of smaller FMD outbreaks in the country, two in 1967, in Hampshire and Warwickshire and one in Northumberland during 1966. The causative agent of all four events was identified as FMD virus (FMDV) serotype O and the source of the large epidemic was attributed to infected bone marrow in lamb products imported from Argentina. However, the diagnostic tools available at the time were unable to entirely rule out connections with the earlier UK FMD outbreaks, as well as other potential sources from Europe. The aim of this study was to apply molecular sequencing to investigate the likely source of this epidemic using VP1 region and full genome (FG) sequences determined directly from clinical epithelium samples (n = 13) or cell culture isolates (n = 6), from this and contemporary outbreaks in the UK, Europe and South America. Analysis of the VP1 sequences provided evidence for at least three separate incursions of FMDV into the UK including one independent introduction that was responsible for the main 1967/68 epidemic. Analysis of FG sequences from the main 1967/68 outbreak (n = 10) revealed nucleotide substitutions at 94 genomic sites providing evidence for the linear accumulation of nucleotide substitutions (rate = 2.42 x 10(-5) nt substitutions/site/day). However, there were five samples where this linear relationship was absent, indicating evolutional dormancy of the virus, presumably outside a host. These results help define the evolutionary dynamics of FMDV during an epidemic and contribute to the knowledge and understanding from which to base future outbreak control strategies.

Iqbal M, Yaqub T, Mukhtar N, Shabbir M Z, McCauley J W (2013)

Infectivity and transmissibility of H9N2 avian influenza virus in chickens and wild terrestrial birds

Veterinary Research 44, e100
Publisher’s version: http://dx.doi.org/10.1186/1297-9716-44-100

Abstract

Genetic changes in avian influenza viruses influence their infectivity, virulence and transmission. Recently we identified a novel genotype of H9N2 viruses in widespread circulation in poultry in Pakistan that contained polymerases (PB2, PB1 and PA) and non-structural (NS) gene segments identical to highly pathogenic H7N3 viruses. Here, we investigated the potential of these viruses to cause disease and assessed the transmission capability of the virus within and between poultry and wild terrestrial avian species. Groups of broilers, layers, jungle fowl, quail, sparrows or crows were infected with a representative strain (A/chicken/UDL-01/08) of this H9N2 virus and then mixed with naive birds of the same breed or species, or different species to examine transmission. With the exception of crows, all directly inoculated and contact birds showed clinical signs, varying in severity with quail showing the most pronounced clinical signs. Virus shedding was detected in all infected birds, with quail showing the greatest levels of virus secretion, but only very low levels of virus were found in directly infected crow samples. Efficient virus intra-species transmission was observed within each group with the exception of crows in which no evidence of transmission was seen. Interspecies transmission was examined between chickens and sparrows and vice versa and efficient transmission was seen in either direction. These results highlight the ease of spread of this group of H9N2 viruses between domesticated poultry and sparrows and show that sparrows need to be considered as a high risk species for transmitting H9N2 viruses between premises.
Jabbar T K, Calvo-Pinilla E, Mateos F, Gubbins S, Bin-Tarif A, Bachanek-Bankowska K, Alpar O, Ortego J, Takamatsu H-H, Mertens P P C, Castillo-Olivares J (2013)

Protection of IFNAR (-/-) mice against bluetongue virus serotype 8, by heterologous (DNA/rMVA) and homologous (rMVA/rMVA) vaccination, expressing outer-capsid protein VP2

PLoS ONE 8 (4), e60574
Publisher’s version: http://dx.doi.org/10.1371/journal.pone.0060574

Abstract

The protective efficacy of recombinant vaccines expressing serotype 8 bluetongue virus (BTV-8) capsid proteins was tested in a mouse model. The recombinant vaccines comprised plasmid DNA or Modified Vaccinia Ankara viruses encoding BTV VP2, VP5 or VP7 proteins. These constructs were administered alone or in combination using either a homologous prime boost vaccination regime (rMVA/rMVA) or a heterologous vaccination regime (DNA/rMVA). The DNA/rMVA or rMVA/rMVA prime-boost were administered at a three week interval and all of the animals that received VP2 generated neutralising antibodies. The vaccinated and non-vaccinated-control mice were subsequently challenged with a lethal dose of BTV-8. Mice vaccinated with VP7 alone were not protected. However, mice vaccinated with DNA/rMVA or rMVA/rMVA expressing VP2, VP5 and VP7 or VP2 alone were all protected.
Jansen C A, de Geus E, van Haarlem D A, van de Haar P M, Londt B Z, Graham S P, Gobel T W, van Eden W, Brookes S M, Vervelde L (2013)

Differential lung NK cell responses in avian influenza virus infected chickens correlate with pathogenicity

Scientific Reports 3, e2478
Publisher’s version: http://dx.doi.org/10.1038/srep02478

Abstract

Infection of chickens with low pathogenicity avian influenza (LPAI) virus results in mild clinical signs while infection with highly pathogenic avian influenza (HPAI) viruses causes death of the birds within 36-48 hours. Since natural killer (NK) cells have been shown to play an important role in influenza-specific immunity, we hypothesise that NK cells are involved in this difference in pathogenicity. To investigate this, the role of chicken NK-cells in LPAI virus infection was studied. Next activation of lung NK cells upon HPAI virus infection was analysed. Infection with a H9N2 LPAI virus resulted in the presence of viral RNA in the lungs which coincided with enhanced activation of lung NK cells. The presence of H5N1 viruses, measured by detection of viral RNA, did not induce activation of lung NK cells. This suggests that decreased NK-cell activation may be one of the mechanisms associated with the enhanced pathogenicity of H5N1 viruses.

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