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Abstract: Infectious bursal disease virus (IBDV) is an important poultry pathogen and is distributed world wide that can cause immune suppression and lesions of the bursa of Fabricius. The main component of the virus, VP2, is not only responsible for the bird''s immune response, but is important for the molecular identification of this virus as well. The nucleic acid of the virus must be adequately preserved to be analyzed by reverse-transcriptase PCR (RT-PCR) and sequenced for the molecular characterization of the field strain. Phenol inactivation has been the standard for IBDV tissue collection and international shipment; however, there have been some reports of interference with molecular detection capabilities when using phenol. Phenol is also a hazardous chemical and must be handled and shipped carefully. The ability to use the Flinders Technology Associates filter paper (FTA® card) for inactivation of several avian pathogens has been proven previously, however no work has been published on its use in IBDV nucleic acid detection. Bursas from experimentally infected birds was imprinted on FTA® cards, and then placed in phenol. Samples were evaluated and compared based on molecular detection capabilities between the two inactivation methods. The nucleic acid of the virus was detected in 85% of the FTA® card inactivated samples compared to 71% in the phenol inactivated samples. Sequence analysis was performed on samples inactivated by both methods and no differences were found. When comparing the RNA stability at different temperatures, euthanized IBDV infected birds were held at two different temperatures before sampling. No differences were detected for FTA® sampling; however, for tissues in phenol the nucleic acid was only detectable up to 2h post-mortem in the tissues held at 4°C prior to sampling. These findings indicate that the FTA® card is an efficient and reliable alternative collection method for molecular detection and characterization of IBDV. [Copyright &y& Elsevier]

Suppressor of cytokine signalling (SOCS) family members are crucial in the control and attenuation of cytokine induced responses via activation of the JAK/STAT, TLR and NF-kB signalling pathways. SOCS proteins orchestrate the termination of many types of immune responses and are often the targets of microbial pathogens exploiting SOCS mechanisms to evade the host's immune response. Through whole and lineage specific genome duplication events, the teleost cytokine/SOCS network is complex. Not only are the orthologues of all mammalian SOCS members present, namely cytokine inducible Src homology 2 (SH2)-containing protein (CISH) and SOCS-1 to -7, but multiple gene copies exist that may potentially become functionally divergent. In this paper we focus on the CISH genes in rainbow trout ( Oncorhynchus mykiss ), and have cloned two further paralogues, CISHa2 and CISHb2, additional to the known CISHa1 and CISHb1 genes. We present for the first time a comparative expression analysis of these four paralogues, to establish whether subfunctionalisation is apparent. In vivo examination of gene expression revealed a higher constitutive expression level of CISHa paralogues compared to CISHb expression in adult trout tissues. All CISHs were relatively highly abundant in immune tissues but CISHa2 and CISHb2 had highest expression in the heart and muscle. An inverse picture of CISH abundance during trout ontogeny was seen, and further hints at differential roles of the four genes in immune regulation and development. Stimulation of head kidney (HK) leukocytes with trout recombinant interleukin (rIL)-15 and rIL-21 had a major effect on CISHa2 and to a lesser extent CISHa1 expression. In HK macrophages rIL-1β, phytohemagglutinin, and phorbol 12-myristate 13-acetate also had a strong impact on CISHa2 expression. Yersinia ruckeri infection caused a temporally and spatially differential onset of CISH expression that may be viewed in the context of pathogen evasion strategies. These data, against the backdrop of fish specific whole genome duplication events and functional divergence, provide the first evidence for differential roles of the four trout CISH genes in immune control and development. [ABSTRACT FROM AUTHOR]

Macrophages mount complex responses to pathogens. Although several key signaling pathways have been identified, it remains unclear how they work together to provide specificity. In a recent paper, Gottschalk et al. report that differential dose–response behaviors of the NFκB and MAPK pathways allow dose-specific gene expression programs. [ABSTRACT FROM AUTHOR]

Abstract: Consider the following stochastic model for immune response. Each pathogen gives birth to a new pathogen at rate . When a new pathogen is born, it has the same type as its parent with probability . With probability , a mutation occurs, and the new pathogen has a different type from all previously observed pathogens. When a new type appears in the population, it survives for an exponential amount of time with mean 1, independently of all the other types. All pathogens of that type are killed simultaneously. Schinazi and Schweinsberg [R.B. Schinazi, J. Schweinsberg, Spatial and non-spatial stochastic models for immune response, Markov Process. Related Fields (2006) (in press)] have shown that this model on behaves rather differently from its non-spatial version. In this paper, we show that this model on a homogeneous tree captures features from both the non-spatial version and the version. We also obtain comparison results, between this model and the basic contact process on general graphs. [Copyright &y& Elsevier]

Abstract: Toxoplasma gondii and Neospora caninum are important causes of reproductive loss in ruminant species worldwide. Both parasites cause disease during pregnancy that may result in foetal death or birth of live congenitally infected offspring. T. gondii is also an important human pathogen with the main risk groups including pregnant women and immuno-compromised individuals, although clinical disease has also been observed in outbreaks among immuno-competent people. While the two parasites are closely related there are distinct differences between the two in their interactions with different host species and subsequent clinical outcome. This paper discusses the respective host–parasite relationships in ovine toxoplasmosis and bovine neosporosis and how the immune response may be host-protective, parasite-protective or contribute to disease pathogenesis, and how this knowledge may help in the development of more effective and targeted vaccination strategies. [Copyright &y& Elsevier]

Abstract: Invading pathogens are controlled by the innate and adaptive arms of the immune system. Adaptive immunity, mediated by B and T lymphocytes, recognises pathogens via high affinity receptors. However, the establishment of a primary adaptive immune response is not rapid enough to eradicate invading microorganisms as it involves cell proliferation, gene activation and protein synthesis. More rapid defence mechanisms are provided by innate immunity, which recognises invading pathogens by germ-line-encoded pattern recognition receptors. Recent evidence shows that this recognition can mainly be attributed to the family of TOLL-like receptors (TLR). Binding of pathogen-associated molecular patterns to TLR induces the production of reactive oxygen and nitrogen intermediates, pro-inflammatory cytokines, and up-regulates expression of co-stimulatory molecules, subsequently initiating the adaptive immunity. In this paper, we will discuss the current knowledge with regards to the TLR, and in particular the bovine family of TLR. In addition, we will show the expression of TLR mRNA in bovine antigen-presenting cell subsets, summarise the discovery and the critical roles of TLR2 in host defence against Mycobacteria, and provide evidence for a mycobacteria species-specific response of bovine macrophages. [Copyright &y& Elsevier]

An animal’s ability to resist disease is usually estimated by measuring one or more components of the immune system. There is an assumption that these assays of immunity measure an animal’s ability to mount an effective immune response. This paper tests this assumption by examining the relationship between two common estimates of insect immunocompetence, phenoloxidase and lysozyme-like enzyme activity, and resistance to three common insect bacterial pathogens: Serratia marcescens, Serratia liquefaciens, and Bacillus cereus. There was a correlation (Spearman’s rs=0.33, p<0.001, n=190 pairs) between total phenoloxidase and baseline lysozyme-like activity within individuals. However, total phenoloxidase and baseline lysozyme-like activity levels did not predict which male crickets would survive any of the three bacterial challenges. Lysozyme-like activity increased after an immune challenge (Friedman, 33.72, p<0.001), and the greater the increase, the greater the chance that the cricket would survive S. marcescens (slope=0.15, χ2=8.2, p=0.005) or B. cereus (slope=0.8, χ2=6.4, p=0.01). The crickets with a greater total hemolymph protein concentration were also more likely to survive a challenge with any of the three bacterial pathogens than the crickets with lower total hemolymph protein concentrations (S. liquefaciens: slope=0.02, χ2=9.2, p=0.002; B. cereus: slope=0.02, χ2=6.5, p=0.01; S. marcescens: slope=0.03, χ2=7.8, p=0.005). Because of the complexity of the immune system, empirical tests of the relationship between assays of immunity and resistance to a range of actual pathogens are important for correctly interpreting these measures. [Copyright &y& Elsevier]

A major challenge for immunologists has been the development of vaccines designed to emphasize cellular immune responses. One particularly promising approach is the prime–boost strategy, which has been shown to generate high levels of T-cell memory in animal models. Recently, several papers have highlighted the power of prime–boost strategies in eliciting protective cellular immunity to a variety of pathogens and have demonstrated efficacy in humans. Coupled with recent advances in our understanding of the mechanisms underlying the generation, maintenance and recall of T-cell memory, the field is poised to make tremendous progress. This Review discusses the impact of these recent developments on the future of prime–boost vaccine strategies. [Copyright &y& Elsevier]

Immune suppression by Treg cells must be overcome to mount robust and effective anti-pathogen immune responses. A new paper in Immunity from Medzhitov and colleagues shows that IL-1-dependent activation of MyD88 promotes the development of Th1 cells by rendering them impervious to Treg cell-mediated inhibition. [ABSTRACT FROM AUTHOR]