Veterinary Science Collected Works - Research Publications

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    Semliki Forest virus strongly reduces mosquito host defence signaling
    Fragkoudis, R ; Chi, Y ; Siu, RWC ; Barry, G ; Attarzadeh-Yazdi, G ; Merits, A ; Nash, AA ; Fazakerley, JK ; Kohl, A (BLACKWELL PUBLISHING, 2008-12)
    The Alphavirus genus within the Togaviridae family contains several important mosquito-borne arboviruses. Other than the antiviral activity of RNAi, relatively little is known about alphavirus interactions with insect cell defences. Here we show that Semliki Forest virus (SFV) infection of Aedes albopictus-derived U4.4 mosquito cells reduces cellular gene expression. Activation prior to SFV infection of pathways involving STAT/IMD, but not Toll signaling reduced subsequent virus gene expression and RNA levels. These pathways are therefore not only able to mediate protective responses against bacteria but also arboviruses. However, SFV infection of mosquito cells did not result in activation of any of these pathways and suppressed their subsequent activation by other stimuli.
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    Properties of non-structural protein 1 of Semliki Forest virus and its interference with virus replication
    Kiiver, K ; Tagen, I ; Zusinaite, E ; Tamberg, N ; Fazakerley, JK ; Merits, A (SOC GENERAL MICROBIOLOGY, 2008-06)
    Semliki Forest virus (SFV) non-structural protein 1 (nsP1) is a major component of the virus replicase complex. It has previously been studied in cells infected with virus or using transient or stable expression systems. To extend these studies, tetracycline-inducible stable cell lines expressing SFV nsP1 or its palmitoylation-negative mutant (nsP16D) were constructed. The levels of protein expression and the subcellular localization of nsP1 in induced cells were similar to those in virus-infected cells. The nsP1 expressed by stable, inducible cell lines or by SFV-infected HEK293 T-REx cells was a stable protein with a half-life of approximately 5 h. In contrast to SFV infection, induction of nsP1 expression had no detectable effect on cellular transcription, translation or viability. Induction of expression of nsP1 or nsP16D interfered with multiplication of SFV, typically resulting in a 5-10-fold reduction in virus yields. This reduction was not due to a decrease in the number of infected cells, indicating that nsP1 expression does not block virus entry or initiation of replication. Expression of nsP1 interfered with virus genomic RNA synthesis and delayed accumulation of viral subgenomic RNA translation products. Expression of nsP1 with a mutation in the palmitoylation site reduced synthesis of genomic and subgenomic RNAs and their products of translation, and this effect did not resolve with time. These results are in agreement with data published previously, suggesting a role for nsP1 in genomic RNA synthesis.
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    Report of the Second External Program and Management Review (EPMR) of The International Livestock Research Institute (ILRI)
    Falvey, J (Consultative Group on International Agricultural Research, 2008)
    THIS DOCUMENT CONTAINS: • Extracts from the Summary Record of Proceedings of the Annual General Meeting 2007 (AGM07) • Science Council Commentary • ILRI Response to the Second ILRI EPMR • Transmittal letter and Report of the Panel on the Second ILRI EPMR
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    Influence of allergen-specific immunotherapy on allergen-specific IgG subclasses in dogs with atopic dermatitis
    Dandrieux, JRS ( 2008-03-03)
    Canine atopic dermatitis (AD) is one of the most common pruritic skin diseases in dogs and is diagnosed based on compatible history, clinical signs and exclusion of other pruritic skin diseases. Allergen-specific immunotherapy (ASIT) is widely used to treat AD but the precise mechanism of action is unknown. The aims of our study were to investigate the influence of ASIT on levels of Dermatophagoides farinae (D. farinae) specific IgG (D. farinae-IgG) subclasses and to explore whether changes in IgG subclasses are associated with the efficacy of ASIT. Sera from 98 dogs were collected before and during ASIT (duration of at least 2 years) with D. farinae. All dogs had serum IgE specific for D. farinae (imovet bg assay). Atopic dogs were divided into two groups: ASIT Group (n=48, ASIT as the sole therapy) and ASIT+ Group (n=50, insufficient control with ASIT requiring additional glucocorticoid treatment). A control group (CTRL Group, n=32) consisted of dogs without dermatological disease. Allergen-specific IgG subclass antibodies were detected by ELISA using monoclonal antibodies specific for canine IgG1 – IgG4. D. farinae-IgG1 and IgG4 were detected in >78% of all sera before ASIT while D. farinae-IgG2 and IgG3 were found in < 31%. Prior to therapy, dogs from the ASIT Group had significantly higher serum D. farinae-IgG1 than dogs in the ASIT+ Group (p<0.05). ASIT led to a significant increase in D. farinae-IgG1 in dogs from the ASIT (p<0.05) and ASIT+ (p<0.01) groups. D. farinae-IgG2, IgG3 and IgG4 concentrations were comparable for all groups before and during ASIT. Allergen-specific IgE concentration was not influenced by ASIT and the concentrations of IgG1 and IgG4 specific to an irrelevant antigen (Betula; birch pollen) were not influenced by ASIT against D. farinae. We conclude that long term ASIT increases levels of D. farinae-IgG1 and that dogs responding well to ASIT have a higher D. farinae-IgG1 concentration before therapy than partial responders.