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

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McCormick J, Flower D R, Strobel S, Wallace D L, Beverley P C L, Tchilian E Z (2003)

Novel perforin mutation in a patient with hemophagocytic lymphohistiocytosis and CD45 abnormal splicing

American Journal of Medical Genetics Part A 117A (3), 255-260


Hemophagocytic lymphohistiocytosis (HLH) composes a group of rare heterogenous disorders characterized by uncontrolled accumulation and infiltration of activated T lymphocytes and macrophages. Cytotoxic T and natural killer cell activity is significantly reduced or absent in these patients. Mutations in the important mediator of lymphocyte cytotoxicity perforin were identified in a number of HLH individuals. Here we report a novel missense mutation thr435met in the conserved Ca2+ binding domain of perforin in a patient with HLH. Prediction of the 3-dimensional structure of the thr435met perforin mutant using comparative molecular modeling indicates that the protein's ability to bind Ca2+, and therefore its cytolytic function, would be strongly compromised. In addition, this patient exhibited abnormal CD45 splicing caused by a C77G mutation in the gene encoding CD45 (PTPRC). Our findings suggest a combined role for perforin mutation and abnormal CD45 splicing as significant contributory factors in the pathogenesis of HLH.
Nunez A, McNeilly F, Perea A, Sanchez-Cordon P J, Huerta B, Allan G, Carrasco L (2003)

Coinfection by Cryptosporidium parvum and porcine circovirus type 2 in weaned pigs

Journal of Veterinary Medicine Series B-Infectious Diseases and Veterinary Public Health 50 (5), 255-258


Routine histopathological diagnosis of one representative 3-month-old pig from a group suffering from diarrhoea revealed a massive degree of parasitation by Cryptosporidium parvum , with a concomitant infection by porcine circovirus type 2 (PCV2), that was confirmed by immunohistochemical procedures. The areas of intestine where parasites were more numerous presented abundant PCV2 infected cells in mucosa and submucosa. The concurrence of C. parvum , a rare primary intestinal pathogen in post-weaning and growing pigs, and PCV2 infections suggest an increased susceptibility as a result of an immunosuppression state.
Paton D J, Parida S, Anderson J (2003)

Detection of FMD infection in vaccinated animals

Report of the session of the Research Group of the Standing Technical Committee of the European Commission for the Control of Foot-and-mouth Disease: Gerzensee, Berne, 16-19 September 2003, Appendix 5 44-51


The purpose of this paper is to briefly review the state of development of tests for the detection of FMD infection in vaccinated animals and the guidelines that are available for their validation and ultimate use. A brief update will be given on studies to develop and evaluate such tests at IAH-Pirbright, in connection to a recent vaccine-challenge experiment.


The aims of this study were to generate chimeric human papillomavirus (HPV)-16 L1 virus-like particles (VLPs) in order to identify immunogenic domains and conformational neutralizing epitopes, and to characterize the regions where a foreign epitope could be introduced. We hypothesized that these regions could be on L1 protein loops since they are exposed on the surface of VLPs. The aims of this study were achieved by mutating HPV-16 L1 proteins. Six amino acids encoding for the epitope 78-83 (DPASRE) of the hepatitis B core (HBc) antigen were introduced within the different loops of the L1 protein at positions 56/57, 140/141, 179/180, 266/267, 283/284 or 352/353. All these chimeric L1 proteins were capable of self-assembly into VLPs. The antigenicity and immunogenicity of some of these VLPs were reduced compared to the levels observed with wild-type VLPs. All were nevertheless able to induce neutralizing antibodies. VLPs with insertion at position 266/267 induced lower levels of neutralizing antibodies, suggesting the involvement of residues situated on FG loop in L1 neutralizing epitopes. All the chimeric L1 proteins except the one with insertion at position 56/57 were also able to induce anti-HBc antibodies, thus suggesting exposure of the HBc epitope on the VLP surface. Taken together, our findings indicate the possibility of designing HPV-derived vectors that are less immunogenic and suggest positions for insertion of defined immune epitopes or cell ligands into L1 protein to be exposed on the surface of VLPs.


The aim of this study was to report on the lesions occurring in the intestine during experimental classical swine fever (CSF) and to clarify the nature of infected cells and the distribution of viral antigen. Thirty-two pigs were inoculated with the virulent CSF virus (CSFV) isolate Alfort 187 and slaughtered from 2 to 15 postinoculation days; four animals of similar background served as a control group. Immunohistochemistry, electron microscopy, and the transferase-mediated deoxyuridine triphosphate nick-end labeling method were used to detect viral antigens and apoptosis. The results showed progressive lymphoid depletion and mucosal necrosis. The lymphoid depletion could have been caused by apoptosis of lymphocytes but could not be directly attributed to the effect of CSFV on these cells. Vascular changes, pathogenic bacteria, and viral infection of epithelial cells were ruled out as causes of necrotic lesions. However, large virally infected monocytes-macrophages with ultrastructural changes indicative of activation were observed in the intestine. This suggests that monocytes-macrophages play an important role in the pathogenesis of intestinal lesions. An understanding of the function of these cells will require additional study.


Previous studies have indicated that the U(L)6, U(L)15, U(L)17, U(L)28, U(L)32, and U(L)33 genes are required for the cleavage and packaging of herpes simplex viral DNA. To identify proteins that interact with the U(L)28-encoded DNA binding protein of herpes simplex virus type 1 (HSV-1), a previously undescribed rabbit polyclonal antibody directed against the U(L)28 protein fused to glutathione S-transferase was used to immunopurify U(L)28 and the proteins with which it associated. It was found that the antibody specifically coimmunoprecipitated proteins encoded by the genes U(L)28, U(L)15, and U(L)33 from lysates of both HEp-2 cells infected with HSV-1(F) and insect cells infected with recombinant baculoviruses expressing these three proteins. In reciprocal reactions, antibodies directed against the U(L)15- or U(L)33-encoded proteins also coimmunoprecipitated the U(L)28 protein. The coimmunoprecipitation of the three proteins from HSV-infected cells confirms earlier reports of an association between the U(L)28 and U(L)15 proteins and represents the first evidence of the involvement of the U(L)33 protein in this complex.

Bautista M J, Ruiz-Villamor E, Salguero F J, Sanchez-Cordon P J, Carrasco L, Gomez-Villamandos J C (2002)

Early platelet aggregation as a cause of thrombocytopenia in classical swine fever

Veterinary Pathology 39 (1), 84-91


Twenty pigs were inoculated with a virulent classical swine fever virus isolate: to determine the mechanism responsible for thrombocytopenia using histopathologic, ultrastructural, and immunohistochemical (detection of viral antigens gp55 and FVIII-rag) techniques. In animals euthanatized at 2, 4, and 6 days post-inoculation (dpi), clusters of granular material staining positive for FVIII-rag were observed in splenic cords, the marginal zone, hepatic sinusoids, and the perisinusoidal space. Moreover, numerous macrophages in these areas were swollen and displayed an intensely positive granular and cytoplasmic reaction. Cell alterations indicative of platelet activation and secretory and phagocytic activation of resident macrophages were also observed in these sites at 2 and 4 dpi. These results suggest that the thrombocytopenia observed in pigs is caused in the first instance by massive activation and subsequent phagocytosis of platelets secondary to the release of platelet-activating factors by activated macrophages.


The major antigenic protein I (MAPI) of the tick-borne rickettsial pathogen Cowdria ruminantium is encoded by a multigene family containing conserved and variable genes. The part of a focus containing the map1 multigene family that was characterized contained three homologous, but non-identical map1 genes, designated mapl1-2, map1-1, and map1. Reverse transcriptase-polymerase chain reaction was used to study the transcriptional activity of these genes in isolates of C ruminantium grown in bovine endothelial cells, in two different tick cell lines, and in Amblyomma variegation ticks. The map1 gene was always transcribed, whereas transcription of map1-2 was not detected under any of the tested conditions. The map1-1 gene transcript was detected in A. variegatum ticks, but was not found in virulent C ruminantium Senegal grown in bovine endothelial cells at 30 or 37degreesC. Interestingly, transcripts of map1-1 were also found in different passages of the in vitro attenuated Senegal isolate grown in bovine endothelial cells, as well as in the Gardel isolate grown in two tick cell lines. When transcribed, map1-1 was present on a polycistronic messenger together with map1.
Bell-Sakyi L, Paxton E, Wright P, Sumption K (2002)

Immunogenicity of Ehrlichia ruminantium grown in tick cell lines

Experimental and Applied Acarology 28 (1), 177-185


Ehrlichia (previously Cowdria) ruminantium, the pathogen which causes heartwater in domestic and wild ruminants, can now be propagated in cell lines from one vector (Amblyomma variegatum) and five non-vector (Ixodes scapularis, I. ricinus, Boophilus decoloratus, B. microplus and Rhipicephalus appendiculatus) tick species. E. ruminantium isolates from West and South Africa and the Caribbean vary in their cell line preference, growth patterns and immunogenic capability. In laboratory trials, certain combinations of tick cell line and E. ruminantium isolate were highly immunogenic in sheep. These trial vaccines were grown under specific in vitro conditions and administered as a single intravenous dose of freshly harvested whole, live culture. Following immunisation and subsequent exposure to virulent E. ruminantium, protected sheep showed no clinical response and a range of serological responses.


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