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        <title>Veterinary Research - Latest Articles</title>
        <link>http://www.veterinaryresearch.org</link>
        <description>The latest research articles published by Veterinary Research</description>
        <dc:date>2012-05-16T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.veterinaryresearch.org/content/43/1/41" />
                                <rdf:li rdf:resource="http://www.veterinaryresearch.org/content/43/1/40" />
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                                <rdf:li rdf:resource="http://www.veterinaryresearch.org/content/43/1/38" />
                                <rdf:li rdf:resource="http://www.veterinaryresearch.org/content/43/1/37" />
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                                <rdf:li rdf:resource="http://www.veterinaryresearch.org/content/43/1/35" />
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        <title>Mannose receptor may be involved in small ruminant lentivirus pathogenesis</title>
        <description>Thirty-one sheep naturally infected with small ruminant lentiviruses (SRLV) of known genotype (A or B), and clinically affected with neurological disease, pneumonia or arthritis were used to analyse mannose receptor (MR) expression (transcript levels) and proviral load in virus target tissues (lung, mammary gland, CNS and carpal joints). Control sheep were SRLV-seropositive asymptomatic (n = 3), seronegative (n = 3) or with chronic listeriosis, pseudotuberculosis or parasitic cysts (n = 1 in each case).  MR expression and proviral load increased with the severity of lesions in most analyzed organs of the SRLV infected sheep and was detected in the affected tissue involved in the corresponding clinical disease (CNS, lung and carpal joint in neurological disease, pneumonia and arthritis animal groups, respectively). The increased MR expression appeared to be SRLV specific and may have a role in lentiviral pathogenesis.</description>
        <link>http://www.veterinaryresearch.org/content/43/1/43</link>
                <dc:creator>Helena Crespo</dc:creator>
                <dc:creator>Paula Jauregui</dc:creator>
                <dc:creator>Idoia Glaria</dc:creator>
                <dc:creator>Letícia San José</dc:creator>
                <dc:creator>Laura Polledo</dc:creator>
                <dc:creator>José F. García-Marín</dc:creator>
                <dc:creator>Lluís Luján</dc:creator>
                <dc:creator>Damián de Andrés</dc:creator>
                <dc:creator>Beatriz Amorena</dc:creator>
                <dc:creator>Ramsés Reina</dc:creator>
                <dc:source>Veterinary Research 2012, null:43</dc:source>
        <dc:date>2012-05-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1297-9716-43-43</dc:identifier>
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                <prism:publicationName>Veterinary Research</prism:publicationName>
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        <prism:startingPage>43</prism:startingPage>
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        <item rdf:about="http://www.veterinaryresearch.org/content/43/1/42">
        <title>Leukocidin genes lukf-P83 and lukM are associated with Staphylococcus aureus clonal complexes 151, 479 and 133 isolated from bovine udder infections in Thuringia, Germany</title>
        <description>Staphylococcus aureus is one of the most important causal agents of bovine mastitis. Population studies on bovine Staphylococcus aureus isolates have identified considerable genetic heterogeneity among strains causing mastitis. The aim of this study was to investigate the contribution of different clonal complexes and the occurrence of virulence factors and resistance determinants within bovine Staphylococcus aureus isolates.A total of 189 Staphylococcus aureus isolates obtained from milk samples of 34 dairy herds in the German Federal State of Thuringia were characterised by microarray technology. The isolates were assigned to eleven different clonal complexes with CC151, CC479 and CC133 being dominant (together 80.5%).The methicillin resistance gene mecA was found in four isolates (2.1%), which belonged to CC398. Enterotoxin genes could be detected in 79.3% of analysed Staphylococcus aureus and 19 isolates (10.1%) harboured a distinct allele of the toxic shock syndrome toxin gene, tst-RF122.The most striking finding of the present study was that almost all except one isolate (151/152) belonging to CC151, CC479 and CC133 harboured the leukocidin genes lukF-P83 and lukM, whereas no further isolates from other lineages possessed these genes. The consistent occurrence of lukF-P83/lukM in the dominating clonal complexes suggests an essential role of this leukocidin in the etiology of bovine mastitis.</description>
        <link>http://www.veterinaryresearch.org/content/43/1/42</link>
                <dc:creator>Katharina Schlotter</dc:creator>
                <dc:creator>Ralf Ehricht</dc:creator>
                <dc:creator>Helmut Hotzel</dc:creator>
                <dc:creator>Stefan Monecke</dc:creator>
                <dc:creator>Martin Pfeffer</dc:creator>
                <dc:creator>Karsten Donat</dc:creator>
                <dc:source>Veterinary Research 2012, null:42</dc:source>
        <dc:date>2012-05-15T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1297-9716-43-42</dc:identifier>
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                <prism:publicationName>Veterinary Research</prism:publicationName>
        <prism:issn>1297-9716</prism:issn>
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        <prism:startingPage>42</prism:startingPage>
        <prism:publicationDate>2012-05-15T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.veterinaryresearch.org/content/43/1/41">
        <title>Suppression of feline coronavirus replication in vitro by cyclosporin A</title>
        <description>The feline infectious peritonitis virus (FIPV) is a member of the feline coronavirus family that causes FIP, which is incurable and fatal in cats. Cyclosporin A (CsA), an immunosuppressive agent that targets the nuclear factor pathway of activated T-cells (NF-AT) to bind cellular cyclophilins (CyP), dose-dependently inhibited FIPV replication in vitro. FK506 (an immunosuppressor of the pathway that binds cellular FK506-binding protein (FKBP) but not CyP) did not affect FIPV replication. Neither cell growth nor viability changed in the presence of either CsA or FK506, and these factors did not affect the NF-AT pathway in fcwf-4 cells. Therefore, CsA does not seem to exert inhibitory effects via the NF-AT pathway. In conclusion, CsA inhibited FIPV replication in vitro and further studies are needed to verify the practical value of CsA as an anti-FIPV treatment in vivo.</description>
        <link>http://www.veterinaryresearch.org/content/43/1/41</link>
                <dc:creator>Yoshikazu Tanaka</dc:creator>
                <dc:creator>Yuka Sato</dc:creator>
                <dc:creator>Shuichi Osawa</dc:creator>
                <dc:creator>Mai Inoue</dc:creator>
                <dc:creator>Satoka Tanaka</dc:creator>
                <dc:creator>Takashi Sasaki</dc:creator>
                <dc:source>Veterinary Research 2012, null:41</dc:source>
        <dc:date>2012-04-30T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1297-9716-43-41</dc:identifier>
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                <prism:publicationName>Veterinary Research</prism:publicationName>
        <prism:issn>1297-9716</prism:issn>
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        <prism:startingPage>41</prism:startingPage>
        <prism:publicationDate>2012-04-30T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.veterinaryresearch.org/content/43/1/40">
        <title>Involvement of the skin during bluetongue virus infection and replication in the ruminant host </title>
        <description>Bluetongue virus (BTV) is a double stranded (ds) RNA virus (genus Orbivirus; family Reoviridae), which is considered capable of infecting all species of domestic and wild ruminants, although clinical signs are seen mostly in sheep. BTV is arthropod-borne (&quot;arbovirus&quot;) and able to productively infect and replicate in many different cell types of both insects and mammalian hosts. Although the organ and cellular tropism of BTV in ruminants has been the subject of several studies, many aspects of its pathogenesis are still poorly understood, partly because of inherent problems in distinguishing between &quot;virus replication&quot; and &quot;virus presence&quot;.BTV replication and organ tropism were studied in a wide range of infected sheep tissues, by immuno-fluorescence-labeling of non-structural or structural proteins (NS2 or VP7 and core proteins, respectively) using confocal microscopy to distinguish between virus presence and replication. These results are compared to gross and microscopic pathological findings in selected organs from infected sheep. Replication was demonstrated in two major cell types: vascular endothelial cells, and agranular leukocytes which morphologically resemble lymphocytes, monocytes/ macrophages and/or dendritic cells. Two organs (the skin and tonsils) were shown to support relatively high levels of BTV replication, although they have not previously been proposed as important replication sites during BTV infection. The high level of BTV replication in the skin is thought to be of major significance for the pathogenesis and transmission of BTV (via biting insects) and a refinement of our current model of BTV pathogenesis is discussed.</description>
        <link>http://www.veterinaryresearch.org/content/43/1/40</link>
                <dc:creator>Karin Darpel</dc:creator>
                <dc:creator>Paul Monaghan</dc:creator>
                <dc:creator>Jennifer Simpson</dc:creator>
                <dc:creator>Simon Anthony</dc:creator>
                <dc:creator>Eva Veronesi</dc:creator>
                <dc:creator>Harriet Brooks</dc:creator>
                <dc:creator>Heather Elliott</dc:creator>
                <dc:creator>Joe Brownlie</dc:creator>
                <dc:creator>Haru-Hisa Takamatsu</dc:creator>
                <dc:creator>Philip Mellor</dc:creator>
                <dc:creator>Peter Mertens</dc:creator>
                <dc:source>Veterinary Research 2012, null:40</dc:source>
        <dc:date>2012-04-30T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1297-9716-43-40</dc:identifier>
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                <prism:publicationName>Veterinary Research</prism:publicationName>
        <prism:issn>1297-9716</prism:issn>
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        <prism:startingPage>40</prism:startingPage>
        <prism:publicationDate>2012-04-30T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.veterinaryresearch.org/content/43/1/39">
        <title>Toxoplasma gondii sexual cross in a single naturally infected feline host: generation of highly mouse-virulent and avirulent clones, genotypically different from clonal types I, II and III</title>
        <description>Tachyzoite clones obtained from a single Toxoplasma gondii oocyst field sample were genotyped and characterized regarding mouse virulence. PCR-RFLP genotyping of tachyzoites initially isolated from interferon-gamma-knockout (GKO) mice, BALB/c mice and VERO cell culture using the nine independent, unlinked genetic markers nSAG2, SAG3, BTUB, GRA6, c22-8, c29-2, L358, PK1 and Apico revealed mixed T. gondii infections showing combinations of type II and type III alleles at different loci. Forty-five individual clones were obtained from all mixed T. gondii tachyzoite cell cultures by limiting dilution. Sixteen T. gondii clones showed type III alleles at all loci and 29 clones displayed a combination of type II and type III alleles at different loci. Five clone groups were identified in total, four of which include T. gondii clones that showed a non-canonical allele pattern and have never been described in natural infections before. All tested clones, except two, were highly virulent in BALB/c mice. The isolation of different non-canonical T. gondii clones originating from an oocyst sample of a single naturally infected cat demonstrate that sexual recombination as well as re-assortment of chromosomes via a sexual cross of T. gondii occur under natural conditions and result in the emergence of clones with increased virulence in mice.</description>
        <link>http://www.veterinaryresearch.org/content/43/1/39</link>
                <dc:creator>Daland Herrmann</dc:creator>
                <dc:creator>Andrea Bärwald</dc:creator>
                <dc:creator>Aline Maksimov</dc:creator>
                <dc:creator>Nikola Pantchev</dc:creator>
                <dc:creator>Majda Vrhovec</dc:creator>
                <dc:creator>Franz Conraths</dc:creator>
                <dc:creator>Gereon Schares</dc:creator>
                <dc:source>Veterinary Research 2012, null:39</dc:source>
        <dc:date>2012-04-30T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1297-9716-43-39</dc:identifier>
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                <prism:publicationName>Veterinary Research</prism:publicationName>
        <prism:issn>1297-9716</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>39</prism:startingPage>
        <prism:publicationDate>2012-04-30T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.veterinaryresearch.org/content/43/1/38">
        <title>Maternal and foetal immune responses of cattle following an experimental challenge with Neospora caninum at day 70 of gestation</title>
        <description>The immune responses of pregnant cattle and their foetuses were examined following inoculation on day 70 of gestation either intravenously (iv) (group 1) or subcutaneously (sc) (group 2) with live NC1 strain tachyzoites or with Vero cells (control) (group 3). Peripheral blood mononuclear cell (PBMC) responses to Neospora antigen and foetal viability were assessed throughout the experiment. Two animals from each group were sacrificed at 14, 28, 42 and 56 days post inoculation (pi). At post mortem, maternal lymph nodes, spleen and PBMC and when possible foetal spleen, thymus and PBMC samples were collected for analysis. Inoculation with NC1 (iv and sc) lead to foetal deaths in all group 1 dams (6/6) and in 3/6 group 2 dams from day 28 pi; statistically significant (p [less than or equal to] 0.05) increases in cell-mediated immune (CMI) responses including antigen-specific cell proliferation and IFN-gamma production as well as increased levels of IL-4, IL-10 and IL-12 were observed in challenged dams compared to the group 3 animals. Lymph node samples from the group 2 animals carrying live foetuses showed greater levels of cellular proliferation as well as significantly (p [less than or equal to] 0.05) higher levels of IFN-gamma compared to the dams in group 2 carrying dead foetuses. Foetal spleen, thymus and PBMC samples demonstrated cellular proliferation as well as IFN-gamma, IL-4, IL-10 and IL-12 production following mitogenic stimulation with Con A from day 14 pi (day 84 gestation) onwards. This study shows that the generation of robust peripheral and local maternal CMI responses (lymphoproliferation, IFN-gamma) may inhibit the vertical transmission of the parasite.</description>
        <link>http://www.veterinaryresearch.org/content/43/1/38</link>
                <dc:creator>Paul Bartley</dc:creator>
                <dc:creator>stephen Wright</dc:creator>
                <dc:creator>Stephen Maley</dc:creator>
                <dc:creator>Colin Macaldowie</dc:creator>
                <dc:creator>Mintu Nath</dc:creator>
                <dc:creator>Clare Hamilton</dc:creator>
                <dc:creator>Frank katzer</dc:creator>
                <dc:creator>David Buxton</dc:creator>
                <dc:creator>Elisabeth Innes</dc:creator>
                <dc:source>Veterinary Research 2012, null:38</dc:source>
        <dc:date>2012-04-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1297-9716-43-38</dc:identifier>
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                <prism:publicationName>Veterinary Research</prism:publicationName>
        <prism:issn>1297-9716</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>38</prism:startingPage>
        <prism:publicationDate>2012-04-26T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.veterinaryresearch.org/content/43/1/37">
        <title>Efficiency of spatio-temporal vaccination regimes in wildlife populations under different viral constraints</title>
        <description>Classical Swine Fever (CSF) is considered an endemic disease in European wild boar populations. In view of the high economic impact of the introduction of the virus into domestic pig units, huge efforts are invested in the preventive control of CSF in wild boar populations. Recent European Community guidelines favour oral mass vaccination against CSF in wild boar populations. The guidelines are explicit on the temporal structure of the vaccination protocol, but little is known about the efficacy of different spatial application schemes, or how they relate to outbreak dynamics.We use a spatially explicit, individual-based wild boar model that represents the ecology of the hosts and the epidemiology of CSF, both on a regional scale and on the level of individual course of infection. We simulate adaptive spatial vaccination schemes accounting for the acute spread of an outbreak while using the temporal vaccination protocol proposed in the Community guidelines.Vaccination was found to be beneficial in a wide range of scenarios. We show that the short-term proactive component of a vaccination strategy is not only as decisive as short-term continuity, but also that it can outcompete alternative practices while being practically feasible. Furthermore, we show that under certain virus-host conditions vaccination might actually contribute to disease persistence in local populations.</description>
        <link>http://www.veterinaryresearch.org/content/43/1/37</link>
                <dc:creator>Martin Lange</dc:creator>
                <dc:creator>Stephanie Kramer-Schadt</dc:creator>
                <dc:creator>Hans-Hermann Thulke</dc:creator>
                <dc:source>Veterinary Research 2012, null:37</dc:source>
        <dc:date>2012-04-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1297-9716-43-37</dc:identifier>
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                <prism:publicationName>Veterinary Research</prism:publicationName>
        <prism:issn>1297-9716</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>37</prism:startingPage>
        <prism:publicationDate>2012-04-24T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.veterinaryresearch.org/content/43/1/36">
        <title>Inability of NS1 protein from an H5N1 influenza virus to activate PI3K/Akt signaling pathway correlates to the enhanced virus replication upon PI3K inhibition</title>
        <description>Phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway, activated during influenza A virus infection, can promote viral replication via multiple mechanisms. Direct binding of NS1 protein to p85beta subunit of PI3K is required for activation of PI3K/Akt signaling. Binding and subsequent activation of PI3K is believed to be a conserved character of influenza A virus NS1 protein. Sequence variation of NS1 proteins in different influenza A viruses led us to investigate possible deviation from the conservativeness. In the present study, NS1 proteins from four different influenza A virus subtypes/strains were tested for their ability to bind p85beta subunit of PI3K and to activate PI3K/Akt. All NS1 proteins efficiently bound to p85beta and activated PI3K/Akt, with the exception of NS1 protein from an H5N1 virus (A/Chicken/Guangdong/1/05, abbreviated as GD05), which bound to p85beta but failed to activate PI3K/Akt, implying that as-yet-unidentified domain(s) in NS1 may alternatively mediate the activation of PI3K. Moreover, PI3K inhibitor, LY294002, did not suppress but significantly increased the replication of GD05 virus. Therefore, our study indicates that activation of PI3K/Akt by NS1 protein is not highly conserved among influenza A viruses and inhibition of the PI3K/Akt pathway as an anti-influenza strategy may not work for all influenza A viruses.</description>
        <link>http://www.veterinaryresearch.org/content/43/1/36</link>
                <dc:creator>Weizhong Li</dc:creator>
                <dc:creator>Gefei Wang</dc:creator>
                <dc:creator>Heng Zhang</dc:creator>
                <dc:creator>Yanqin Shen</dc:creator>
                <dc:creator>Jianping Dai</dc:creator>
                <dc:creator>Liqi Wu</dc:creator>
                <dc:creator>Jianxiang Zhou</dc:creator>
                <dc:creator>Zhiwu Jiang</dc:creator>
                <dc:creator>Kangsheng Li</dc:creator>
                <dc:source>Veterinary Research 2012, null:36</dc:source>
        <dc:date>2012-04-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1297-9716-43-36</dc:identifier>
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                <prism:publicationName>Veterinary Research</prism:publicationName>
        <prism:issn>1297-9716</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>36</prism:startingPage>
        <prism:publicationDate>2012-04-24T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.veterinaryresearch.org/content/43/1/35">
        <title>The fungal T-2 toxin alters the activation of primary macrophages induced by TLR-agonists resulting in a decrease of the inflammatory response in the pig</title>
        <description>T-2 toxin is known to be one of the most toxic trichothecene mycotoxins. Exposure to T-2 toxin induces many hematologic and immunotoxic disorders and is involved in immuno-modulation of the innate immune response. The objective of this work was to evaluate the effects of T-2 toxin on the activation of macrophages by different agonists of Toll-like receptors (TLR) using an in vitro model of primary porcine alveolar macrophages (PAM). Cytotoxic effects of T-2 toxin on PAM were first evaluated. An IC50 of 19.47 +/- 0.9753 nM was determined for the cytotoxicity of T-2 toxin. A working concentration of 3 nM of T-2 toxin was chosen to test the effect of T-2 toxin on TLR activation; this dose was not cytotoxic and did not induce apoptosis as demonstrated by Annexin/PI staining. A pre-exposure of macrophages to 3 nM of T-2 toxin decreased the production of inflammatory mediators (IL-1 beta, TNF-alpha, nitric oxide) in response to LPS and FSL1, TLR4 and TLR2/6 agonists respectively. The decrease of the pro-inflammatory response is associated with a decrease of TLR mRNA expression. By contrast, the activation of TLR7 by ssRNA was not modulated by T-2 toxin pre-treatment. In conclusion, our results suggest that ingestion of low concentrations of T-2 toxin affects the TLR activation by decreasing pattern recognition of pathogens and thus interferes with initiation of inflammatory immune response against bacteria and viruses. Consequently, mycotoxins could increase the susceptibility of humans and animals to infectious diseases.</description>
        <link>http://www.veterinaryresearch.org/content/43/1/35</link>
                <dc:creator>Julie Seeboth</dc:creator>
                <dc:creator>Romain Solinhac</dc:creator>
                <dc:creator>Isabelle Oswald</dc:creator>
                <dc:creator>Laurence Guzylack-Piriou</dc:creator>
                <dc:source>Veterinary Research 2012, null:35</dc:source>
        <dc:date>2012-04-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1297-9716-43-35</dc:identifier>
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                <prism:publicationName>Veterinary Research</prism:publicationName>
        <prism:issn>1297-9716</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>35</prism:startingPage>
        <prism:publicationDate>2012-04-24T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.veterinaryresearch.org/content/43/1/34">
        <title>The effect of exogenous corticosterone on West Nile virus infection in Northern Cardinals (Cardinalis cardinalis)</title>
        <description>The relationship between stress and disease is thought to be unambiguous: chronic stress induces immunosuppression, which likely increases the risk of infection. However, this link has not been firmly established in wild animals, particularly whether stress hormones affect host responses to zoonotic pathogens, which can be transmitted to domesticated animal, wildlife and human populations. Due to the dynamic effects of stress hormones on immune functions, stress hormones may make hosts better or poorer amplifying hosts for a pathogen contingent on context and the host species evaluated. Using an important zoonotic pathogen, West Nile virus (WNV) and a competent host, the Northern Cardinal (Cardinalis cardinalis), we tested the effects of exogenous corticosterone on response to WNV infection. Corticosterone was administered at levels that individuals enduring chronic stressors (i.e., long-term inclement weather, food shortage, anthropogenic pollution) might experience in the wild. Corticosterone greatly impacted mortality: half of the corticosterone-implanted cardinals died between five - 11 days post-inoculation whereas only one of nine sham-implanted (control) birds died. No differences were found in viral titer between corticosterone- and sham-implanted birds. However, cardinals that survived infections had significantly higher average body temperatures during peak infection than individuals that died. In sum, this study indicates that elevated corticosterone could affect the survival of WNV-infected wild birds, suggesting that populations may be disproportionately at-risk to disease in stressful environments.</description>
        <link>http://www.veterinaryresearch.org/content/43/1/34</link>
                <dc:creator>Jennifer Owen</dc:creator>
                <dc:creator>Ayaka Nakamura</dc:creator>
                <dc:creator>Courtney Coon</dc:creator>
                <dc:creator>Lynn Martin</dc:creator>
                <dc:source>Veterinary Research 2012, null:34</dc:source>
        <dc:date>2012-04-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1297-9716-43-34</dc:identifier>
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                <prism:publicationName>Veterinary Research</prism:publicationName>
        <prism:issn>1297-9716</prism:issn>
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        <prism:startingPage>34</prism:startingPage>
        <prism:publicationDate>2012-04-21T00:00:00Z</prism:publicationDate>
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