A mechanistic basis for the co-evolution of chicken tapasin and major histocompatibility complex class I (MHC I) proteins.

MHC class I molecules display peptides at the cell surface to cytotoxic T cells. The co-factor tapasin functions to ensure that MHC I becomes loaded with high affinity peptides. In most mammals, the tapasin gene appears to have little sequence diversity and few alleles and is located distal to several classical MHC I loci, so tapasin appears to function in a universal way to assist MHC I peptide loading.

Differential effects of viral vectors on migratory afferent lymph dendritic cells in vitro predict enhanced immunogenicity in vivo.

Targeting dendritic cells (DC) is key to driving effective immune responses. Lymphatic cannulation provides access to the heterogeneous populations of DC draining peripheral sites in rodents and ruminants. Afferent lymph DEC-205(+) CD11c(+) SIRPα(+) DC were preferentially infected ex vivo with three vaccine viral vectors: recombinant human replication-defective human adenovirus 5 (rhuAdV5), recombinant modified vaccinia virus Ankara (rMVA), and recombinant fowlpox virus (rFPV), all expressing green fluorescent protein (GFP).

Bovine plasmacytoid dendritic cells are the major source of type I interferon in response to foot-and-mouth disease virus in vitro and in vivo.

Type I interferons (alpha/beta interferons [IFN-α/β]) are the main innate cytokines that are able to induce a cellular antiviral state, thereby limiting viral replication and disease pathology. Plasmacytoid dendritic cells (pDCs) play a crucial role in the control of viral infections, especially in response to viruses that have evolved mechanisms to block the type I IFN signal transduction pathway. Using density gradient separation and cell sorting, we have highly enriched a population of bovine cells capable of producing high levels of biologically active type I IFN.

The CD2v protein enhances African swine fever virus replication in the tick vector, Ornithodoros erraticus.

The NH/P68 non-haemadsorbing (non-HAD) African swine fever virus (ASFV) isolate contains frameshift mutations in the EP402R and adjacent EP153R genes. These encode, respectively, the protein (CD2v) that is required for the haemadsorption (HAD) of swine erythrocytes to ASFV-infected cells and a C-type lectin protein. Two recombinant HAD viruses were constructed in this parental strain.

Airborne spread of foot-and-mouth disease--model intercomparison.

Foot-and-mouth disease virus (FMDV) spreads by direct contact between animals, by animal products (milk, meat and semen), by mechanical transfer on people or fomites and by the airborne route, with the relative importance of each mechanism depending on the particular outbreak characteristics. Atmospheric dispersion models have been developed to assess airborne spread of FMDV in a number of countries, including the UK, Denmark, Australia, New Zealand, USA and Canada. These models were compared at a Workshop hosted by the Institute for Animal Health/Met Office in 2008.

WITHDRAWN: Foot-and-mouth disease: How much airborne virus do animals exhale?

This article has been withdrawn at the request of the Editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.

Route of challenge is critical in determining the clinical outcome of infection with a very virulent oncogenic herpesvirus, Marek's disease virus.

The majority of experimental studies examining Marek's disease virus infection have used parenteral injection of cell-associated virus. The aim of this study was to examine whether the route of entry of virus was critical in determining the outcome of infection. Susceptible (L7) and resistant (L6) White Leghorn chickens were infected with a very virulent Marek's disease virus, RB1B, by either the intra-abdominal or intra-tracheal route.

'Rescue' of mini-genomic constructs and viruses by combinations of morbillivirus N, P and L proteins.

Chloramphenicol acetyltransferase (CAT)-expressing negative-sense mini-genomic constructs of measles virus (MV) and rinderpest virus (RPV) were rescued by standard technology with helper plasmids expressing the nucleocapsid (N), phospho- (P) and large (L) proteins of MV, canine distemper virus (CDV) or RPV in order to determine whether the proteins of different viruses can function together. Homogeneous sets consisting of N, P and L plasmids derived from one virus were able to generate reporter gene expression from either mini-genomic construct. Heterogeneous sets of proteins from different viruses were not functional, with the exception that a low level of activity was obtained when MV N and P protein were combined with RPV L protein in the rescue of the MV mini-genomic construct, or CDV N was combined with RPV P and L in the rescue of the RPV mini-genome.

Making a vaccinate-to-live policy a reality in foot-and-mouth disease.

Public opinion and the availability of new technologies are making the use of 'stamping- out' an increasingly unattractive option as the method of first choice for foot-and-mouth disease (FMD) control in FMD-free countries or zones seeking to control incursion of disease. There is therefore increasing pressure to adopt a 'vaccinate-to-live' policy in these circumstances. For a successful vaccinate-to-live policy, veterinary services need access to appropriate, licensed vaccines; to have adequate contingency plans to ensure that they can deliver the required vaccine, where and when it is needed; and to have developed an 'exit strategy' that enables recognition of freedom from disease as quickly as possible.

Isolation and characterization of a mutant strain of Streptococcus uberis, which fails to utilize a plasmin derived beta-casein peptide for the acquisition of methionine.

Aims: To isolate and characterize a mutant of Streptococcus uberis strain 0140J which fails to utilize a plasmin derived beta-casein peptide for the acquisition of methionine.

Methods And Results: Random insertional mutagenesis was used to isolate a mutant strain of Strep. uberis 0140J which was unable to utilize methionine from within a casein-derived peptide.

Pathogenesis and diagnosis of infections with Mycobacterium bovis in cattle. Independent Scientific Group on Cattle TB.

In last week's Veterinary Record, members of the Independent Scientific Group on Cattle TB discussed the approach they are adopting in attempting to develop sustainable strategies for controlling bovine tuberculosis in cattle (VR, February 19, pp 207-210). In this second, complementary article, they consider the extent to which efforts to control the disease may be constrained by limitations in current testing procedures.

Transient expression of beta-galactosidase in differentiating sporozoites of Eimeria tenella.

A transient transfection system has been developed for a member of the Apicomplexa, Eimeria tenella, using beta-galactosidase (betagal) from Escherichia coli as the reporter enzyme. Successfully expressed constructs contained sequences of the E. tenella microneme gene Etmic-1 fused to the coding region of lacZ.

Identification of two distinct populations of dendritic cells in afferent lymph that vary in their ability to stimulate T cells.

Immunofluorescent staining and flow cytometric analysis of dendritic cells from cattle afferent lymph has established that within the afferent lymph veiled cells (ALVC) there are two phenotypically distinct, major populations. One is CD11a+, CD5+, CD21- and expresses the bovine WC10 (workshop cluster 10) molecule and the Ag recognized by mAb CC81 but is not recognized by mAbs CC149 and IL-A24. The second ALVC subpopulation is CD11a-, CD5-, CD21+/-, workshop cluster 10- and is not recognized by mAb CC81 but is recognized by mAb CC149.

Rinderpest: at war with the disease of war.

Rinderpest, the legendary cattle plague, has caused devastating losses for centuries and remains the biggest threat to sustainable livestock production in developing countries. Strenuous efforts are now being made to achieve global eradication of this viral disease, a goal made feasible through the use of attenuated live vaccines developed in the 1950s. Their use almost resulted in eradication in the 1970s but left several foci of disease from where the plague then re-emerged.