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

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Webb P R, Powell L, Denyer M, Marsh S, Weaver C, Simmons M M, Johns E, Sheehan J, Horsfield P, Lyth C, Wilson C, Long A, Cawthraw S, Saunders G C, Spencer Y I (2009)

A retrospective immunohistochemical study reveals atypical scrapie has existed in the United Kingdom since at least 1987

Journal of Veterinary Diagnostic Investigation 21 (6), 826-829
Publisher’s version: http://dx.doi.org/10.1177/104063870902100609

Abstract

Atypical scrapie is a relatively recent discovery, and it was unknown whether it was a new phenomenon or whether it had existed undetected in the United Kingdom national flock. Before 1998, the routine statutory diagnosis of transmissible spongiform encephalopathy (TSE) in sheep relied on the presence of TSE vacuolation in the brainstem. This method would not have been effective for the detection of atypical scrapie. Currently, immunohistochemistry (IHC) and Western blot are commonly used for the differential diagnosis of classical and atypical scrapie. The IHC pattern of PrP(d) deposition in atypical scrapie is very different from that in classical scrapie using the same antibody. It is thus possible that because of a lack of suitable diagnostic techniques and awareness of this form of the disease, historic cases of atypical scrapie remain undiagnosed. Immunohistochemistry was performed on selected formalin-fixed, paraffin-embedded (FFPE) blocks of ovine brain from the Veterinary Laboratories Agency archives that were submitted for various reasons, including suspect neurological disorders, between 1980 and 1989. It was found that PrP(d) deposits in a single case were consistent with atypical scrapie. A method was developed to obtain a PrP genotype from FFPE tissues and was applied to material from this single case, which was shown to be AHQ/AHQ. This animal was a scrapie suspect from 1987, but diagnosis was not confirmed by the available techniques at that time.
Wilson A, Mellor P S, Szmaragd C, Mertens P P C (2009)

Adaptive strategies of African horse sickness virus to facilitate vector transmission

Veterinary Research 40 (2), 16
Publisher’s version: http://dx.doi.org/10.1051/vetres:2008054

Abstract

African horse sickness virus (AHSV) is an orbivirus that is usually transmitted between its equid hosts by adult Culicoides midges. In this article, we review the ways in which AHSV may have adapted to this mode of transmission. The AHSV particle can be modified by the pH or proteolytic enzymes of its immediate environment, altering its ability to infect different cell types. The degree of pathogenesis in the host and vector may also represent adaptations maximising the likelihood of successful vectorial transmission. However, speculation upon several adaptations for vectorial transmission is based upon research on related viruses such as bluetongue virus (BTV), and further direct studies of AHSV are required in order to improve our understanding of this important virus.
Wilson A J, Mellor P S (2009)

Bluetongue in Europe: past, present and future

Philosophical Transactions of the Royal Society B-Biological Sciences 364 (1530), 2669-2681
Publisher’s version: http://dx.doi.org/10.1098/rstb.2009.0091

Abstract

The recent arrival in Northern and Western (NW) Europe of bluetongue virus (BTV), which causes the ruminant disease ‘bluetongue’, has raised the profile of this vector-borne ruminant disease and sparked discussions on the reasons for its sudden emergence so far north. This expansion has not happened in isolation and the disease has been expanding into Southern and Eastern Europe for the last decade. This shifting disease distribution is being facilitated by a number of different introduction mechanisms including the movement of infected livestock, the passive movement of infected Culicoides on the wind and, in NW Europe, an unknown route of introduction. The expansion of BTV in Europe has forced a re-evaluation of the importance of Palaearctic Culicoides species in transmission, as well as the importance of secondary transmission routes, such as transplacental transmission, in facilitating the persistence of the virus. The current European outbreak of BTV-8 is believed to have caused greater economic damage than any previous single-serotype outbreak. Although attempts are being made to improve the capacity of European countries to cope with future BTV incursions, the options available are limited by a lack of basic entomological data and limited virological surveillance.
Yao Y, Zhao Y, Smith L P, Watson M, Nair V (2009)

Novel microRNAs (miRNAs) encoded by herpesvirus of Turkeys: evidence of miRNA evolution by duplication

Journal of Virology 83 (13), 6969-6973
Publisher’s version: http://dx.doi.org/10.1128/JVI.00322-09

Abstract

Herpesviruses account for 134 out of the 140 virus-encoded microRNAs (miRNAs) known today. Here we report the identification of 11 novel miRNAs encoded by herpesvirus of turkey (HVT), a virus used as a live vaccine in poultry against the highly oncogenic Marek's disease virus type 1. Ten of these miRNAs were clustered together within the repeat long region of the viral genome, demonstrating some degree of positional conservation with other mardiviruses. Close sequence and phylogenetic relationships of some miRNAs in this cluster indicate evolution by duplication. HVT miRNAs represent the first example of virus-encoded miRNAs that show evolution by duplication.
Almolda B, Costa M, Montoya M, Gonzalez B, Castellano B (2009)

CD4 microglial expression correlates with spontaneous clinical improvement in the acute Lewis rat EAE model

Journal of Neuroimmunology 209 (1-2), 65-80
Publisher’s version: http://dx.doi.org/10.1016/j.jneuroim.2009.01.026

Abstract

CD4 is a molecule commonly expressed on the surface of T-helper lymphocytes with a recognized critical role in the antigen presentation process that has also been reported in monocytes and macrophages, although its role in these cells remains unknown. The objective of the present study was to analyze whether experimental conditions involving a potent acquired immune component, as occurs in experimental autoimmune encephalomyelitis (EAE), are able to induce CD4 expression in the population of microglia/macrophages. Myelin Basic Protein (MBP) immunized female Lewis rats, were examined at different phases during the course of EAE according to their clinical score. Spinal cords were analyzed by flow cytometry for CD11b, CD4 and CD45, by histochemistry for NDPase and by immunohistochemistry for ED2, Iba1, CD45 and CD4. Flow cytometry analysis showed that EAE induced CD4 expression in macrophages (CD11b+/CD45(high)) and microglia (in both CD11b+/CD45(intermediate) and CD11b+/CD45(low) phenotypes). Noticeably, microglial CD4 expression was found during the recovery phase and was maintained until 40 days post-induction. In agreement, immunolabelled sections revealed CD4 expression in microglial cells with ramified morphology during the recovery and post-recovery phases. In conclusion, our results indicate that, in this EAE model, perivascular cells, microglia and macrophages showed different dynamics during the course of the disease in close relation with symptomatology and that microglial cells expressed CD4 interestingly during the recovery phase, suggesting a role of microglial CD4 expression in the resolution of the immune response.
Anthony S J, Maan S, Maan N, Kgosana L, Bachanek-Bankowska K, Batten C, Darpel K E, Sutton G, Attoui H, Mertens P P C (2009)

Genetic and phylogenetic analysis of the outer-coat proteins VP2 and VP5 of epizootic haemorrhagic disease (EHDV): comparison of genetic and serological data to characterise the EHDV serogroup

Virus Research 145 (2), 200-210
Publisher’s version: http://dx.doi.org/10.1016/j.virusres.2009.07.012

Abstract

The outer-coat proteins, VP2 and VP5, of epizootic haemorrhagic disease virus (EHDV) are important for host cell binding during the initiation of infection. They are also known to determine virus serotype. This study presents a complete genetic and phylogenetic analysis of these proteins (and the genes that code for them) to allow comparison of the selective pressures acting on each and the correlation of genetic sequence data with serotype. Accession numbers, gene and protein sizes, ORF positions, G+C contents, terminal hexanucleotides, start and stop codons and phylogenetic relationships are all presented. The results show that VP2 is highly variable, is under great pressure to adapt and can be correlated with serotype. While also variable, VP5 appears to be under less adaptive pressure than VP2 but still shows some correlation with serotype. Seven serotypes of EHDV have been defined in this study, although the results do show that some serotypes are extremely closely related—and highlight the benefit of using both molecular and serologic analyses. Analysis of the terminal hexanucleotides showed that the 5? terminus is under greater purifying selection than the 3?. Evidence is also presented that both segments 2 and 6 (coding for VP2 and VP5 respectively) have grown via gene duplication and subsequent mutation.
Armesto M, Cavanagh D, Britton P (2009)

The replicase gene of avian coronavirus infectious bronchitis virus is a determinant of pathogenicity

PLoS One 4 (10), e7384
Publisher’s version: http://dx.doi.org/10.1371/journal.pone.0007384

Abstract

We have previously demonstrated that the replacement of the S gene from an avirulent strain (Beaudette) of infectious bronchitis virus (IBV) with an S gene from a virulent strain (M41) resulted in a recombinant virus (BeauR-M41(S)) with the in vitro cell tropism of the virulent virus but that was still avirulent. In order to investigate whether any of the other structural or accessory genes played a role in pathogenicity we have now replaced these from the Beaudette strain with those from M41. The recombinant IBV was in effect a chimaeric virus with the replicase gene derived from Beaudette and the rest of the genome from M41. This demonstrated that it is possible to exchange a large region of the IBV genome, approximately 8.4 kb, using our transient dominant selection method. Recovery of a viable recombinant IBV also demonstrated that it is possible to interchange a complete replicase gene as we had in effect replaced the M41 replicase gene with the Beaudette derived gene. Analysis of the chimaeric virus showed that it was avirulent indicating that none of the structural or accessory genes derived from a virulent isolate of IBV were able to restore virulence and that therefore, the loss of virulence associated with the Beaudette strain resides in the replicase gene.
Attarzadeh-Yazdi G, Fragkoudis R, Chi Y, Siu R W, Ulper L, Barry G, Rodriguez-Andres J, Nash A A, Bouloy M, Merits A, Fazakerley J K, Kohl A (2009)

Cell-to-cell spread of the RNA interference response suppresses Semliki Forest virus (SFV) infection of mosquito cell cultures and cannot be antagonized by SFV

Journal of Virology 83 (11), 5735-5748
Publisher’s version: http://dx.doi.org/10.1128/jvi.02440-08

Abstract

In their vertebrate hosts, arboviruses such as Semliki Forest virus (SFV) (Togaviridae) generally counteract innate defenses and trigger cell death. In contrast, in mosquito cells, following an early phase of efficient virus production, a persistent infection with low levels of virus production is established. Whether arboviruses counteract RNA interference (RNAi), which provides an important antiviral defense system in mosquitoes, is an important question. Here we show that in Aedes albopictus-derived mosquito cells, SFV cannot prevent the establishment of an antiviral RNAi response or prevent the spread of protective antiviral double-stranded RNA/small interfering RNA (siRNA) from cell to cell, which can inhibit the replication of incoming virus. The expression of tombusvirus siRNA-binding protein p19 by SFV strongly enhanced virus spread between cultured cells rather than virus replication in initially infected cells. Our results indicate that the spread of the RNAi signal contributes to limiting virus dissemination.
Ayelet G, Mahapatra M, Gelaye E, Egziabher B G, Rufeal T, Sahle M, Ferris N P, Wadsworth J, Hutchings G H, Knowles N J (2009)

Genetic characterization of foot-and-mouth disease viruses (FMDV) , Ethiopia, 1981-2007

Emerging Infectious Diseases 15 (9), 1409-1417
Publisher’s version: http://dx.doi.org/10.3201/eid1509.090091

Abstract

Foot-and-mouth disease (FMD) is endemic to sub-Saharan Africa. To further understand its complex epidemiology, which involves multiple virus serotypes and host species, we characterized the viruses recovered from FMD outbreaks in Ethiopia during 1981–2007. We detected 5 of the 7 FMDV serotypes (O, A, C, Southern African Territories [SAT] 1, and SAT 2). Serotype O predominated, followed by serotype A; type C was not recognized after 1983. Phylogenetic analysis of virus protein 1 sequences indicated emergence of a new topotype within serotype O, East Africa 4. In 2007, serotype SAT 1 was detected in Ethiopia and formed a new distinct topotype (IX), and serotype SAT 2 reappeared after an apparent gap of 16 years. The diversity of viruses highlights the role of this region as a reservoir for FMD virus, and their continuing emergence in Ethiopia will greatly affect spread and consequent control strategy of the disease on this continent.
Ayora-Talavera G, Shelton H, Scull M A, Ren J, Jones I M, Pickles R J, Barclay W S (2009)

Mutations in H5N1 influenza virus hemagglutinin that confer binding to human tracheal airway epithelium

PLoS One 4 (11), e7836
Publisher’s version: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2775162/

Abstract

The emergence in 2009 of a swine-origin H1N1 influenza virus as the first pandemic of the 21st Century is a timely reminder of the international public health impact of influenza viruses, even those associated with mild disease. The widespread distribution of highly pathogenic H5N1 influenza virus in the avian population has spawned concern that it may give rise to a human influenza pandemic. The mortality rate associated with occasional human infection by H5N1 virus approximates 60%, suggesting that an H5N1 pandemic would be devastating to global health and economy. To date, the H5N1 virus has not acquired the propensity to transmit efficiently between humans. The reasons behind this are unclear, especially given the high mutation rate associated with influenza virus replication. Here we used a panel of recombinant H5 hemagglutinin (HA) variants to demonstrate the potential for H5 HA to bind human airway epithelium, the predominant target tissue for influenza virus infection and spread. While parental H5 HA exhibited limited binding to human tracheal epithelium, introduction of selected mutations converted the binding profile to that of a current human influenza strain HA. Strikingly, these amino-acid changes required multiple simultaneous mutations in the genomes of naturally occurring H5 isolates. Moreover, H5 HAs bearing intermediate sequences failed to bind airway tissues and likely represent mutations that are an evolutionary "dead end." We conclude that, although genetic changes that adapt H5 to human airways can be demonstrated, they may not readily arise during natural virus replication. This genetic barrier limits the likelihood that current H5 viruses will originate a human pandemic.

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