91 research outputs found
Rabbit haemorrhagic disease: experimental study of a recent highly pathogenic GI.2/RHDV2/b strain and evaluation of vaccine efficacy
[EN] In 2010, a variant of the rabbit haemorrhagic disease virus (RHDV) belonging to a new GI.2 genotype was identified in France and rapidly spread worldwide. Due to antigenic difference, new vaccines including G1.2 strains have been developed to confer adequate protection. An increase in the pathogenicity of the circulating strains was recently reported. The objective of this experimental study was to characterise the infection with a highly pathogenic GI.2/RHDV2/b isolate (2017) and assess the efficacy of Filavac VHD K C+V vaccine (Filavie) against this strain. Four and 10-wk-old specific pathogen-free rabbits were inoculated with a recommended dose of vaccine. After 7 d, controls and vaccinated rabbits were challenged and clinically monitored for 14 d. All animals were necropsied and blood, organs and urine were sampled for quantitative reverse transcription polymerase chain reaction (RT-qPCR) analysis. In adult groups, regular nasal and rectal swabbing were performed, and faeces were collected after death to monitor RNA shedding. In control groups, the challenge strain induced acute RHD between 31 and 72 h post-inoculation, with a mortality rate of 100% for kits and 89% for adult rabbits. Except for a shorter mean time to death in kits, similar clinical signs and lesions were observed between age groups. The vaccination significantly prevented all mortality, clinical signs, detection of viral RNA in serum and gross lesions in kits and adult rabbits. In adult groups, we also demonstrated that vaccine significantly protected from detectable RNA shedding via naso-conjunctival and rectal routes. Two weeks after challenge, RNA copies were not detected by PCR in the liver, spleen, lungs, kidneys, faeces and urine of vaccinated adult rabbits. The findings for kits were similar, except that very low levels of RNA were present in the liver and spleen of a few rabbits. These data show that immunisation prevented any significant viral multiplication and/or allowed a rapid clearance. We concluded that, despite the quick evolution of GI.2/RHDV2/b strains, the protection conferred by the vaccine remains adequate. In the context of coexistence of both GI.1 and GI.2 genotypes in some countries, with the circulation of multiples recombinant viruses, the vaccination should be based on the association of strains from both genotypes.Le Minor, O.; Boucher, S.; Joudou, L.; Mellet, R.; Sourice, M.; Le Moullec, T.; Nicolier, A.... (2019). Rabbit haemorrhagic disease: experimental study of a recent highly pathogenic GI.2/RHDV2/b strain and evaluation of vaccine efficacy. World Rabbit Science. 27(3):143-156. https://doi.org/10.4995/wrs.2019.11082SWORD143156273Abrantes J., van der Loo W., Le Pendu J., Esteves P.J. 2012. Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review. Vet. Res., 43: 12. https://doi.org/10.1186/1297-9716-43-12Abrantes J., Lopes A.M., Dalton K.P., Melo P., Correia J.J., Ramada M., Alves P.C., Parra F., Esteves P.J. 2013. New variant of rabbit hemorrhagic disease virus, Portugal, 2012-2013. Emerg. Infect. Dis., 19: 1900-1902. https://doi.org/10.3201/eid1911.130908Calvete C., Sarto P., Calvo A.J., Monroy F., Calvo J.H. 2014. Letter - Could the new rabbit haemorrhagic disease virus variant (RHDVb) be fully replacing classical RHD strains in the Iberian Peninsula?. World Rabbit Sci., 22: 91-91. https://doi.org/10.4995/wrs.2014.1715Calvete C, Mendoza M, Alcaraz A, Sarto M.P., JimĂ©nez-de-BagĂŒĂ©ss M.P., Calvo A.J., Monroy F., Calvo J.H., 2018. Rabbit haemorrhagic disease: Cross-protection and comparative pathogenicity of GI.2/RHDV2/b and GI.1b/RHDV lagoviruses in a challenge trial. Vet. Microbiol., 219: 87-95. https://doi.org/10.1016/j.vetmic.2018.04.018Capucci L., Cavadini P., Schiavitto M., Lombardi G., Lavazza A. 2017. Increased pathogenicity in rabbit haemorrhagic disease virus type 2 (RHDV2). Vet. Rec., 180: 426. https://doi.org/10.1136/vr.104132Carvalho C.L., Duarte E.L., Monteiro M., Botelho A., Albuquerque T., Fevereiro M., Henriques A.M., Barros SS., Duarte MD. 2017. Challenges in the rabbit haemorrhagic disease 2 (RHDV2) molecular diagnosis of vaccinated rabbits. Vet. Microbiol. 198: 43-50. https://doi.org/10.1016/j.vetmic.2016.12.006Dalton K.P., Balseiro A., Juste R.A., Podadera A., Nicieza I., Del Llano D., GonzĂĄlez R., Martin Alonso J.M., Prieto J.M., Parra F., Casais R. 2018. Clinical course and pathogenicity of variant rabbit haemorrhagic disease virus in experimentally infected adult and kit rabbits: Significance towards control and spread. Vet. Microbiol., 220: 24-32. https://doi.org/10.1016/j.vetmic.2018.04.033Dalton K.P., Nicieza I., Abrantes J., Esteves P.J., Parra F., 2014. Spread of new variant RHDV in domestic rabbits on the Iberian Peninsula. Vet. Microbiol., 169: 67-73. https://doi.org/10.1016/j.vetmic.2013.12.015Dalton K.P., Nicieza I., Balseiro A., Muguerza M.A., Rosell J.M., Casais R., Ălvarez Ă.L., Parra F. 2012. Variant rabbit hemorrhagic disease virus in young rabbits, Spain. Emerg. Infect. Dis., 18: 2009-2012. https://doi.org/10.3201/eid1812.120341Duarte M., Henriques M., Barros S.C., Fagulha T., Ramos F., LuĂs T., Fevereiro M., Benevides S., Flor L., Barros S.V., Bernardo S. 2015. Detection of RHDV variant 2 in the Azores. Vet. Rec.,176: 130. https://doi.org/10.1136/vr.h497Forrester N.L., Boag B., Moss S.R., Turner S.L., Trout R.C., White P.J., Hudson P.J., Gould E.A., 2003. Long-term survival of New Zealand rabbit haemorrhagic disease virus RNA in wild rabbits, revealed by RT-PCR and phylogenetic analysis. J. Gen.Virol., 84: 3079-3086. https://doi.org/10.1099/vir.0.19213-0Gall A., Schirrmeier H. 2006. Persistence of rabbit haemorrhagic disease virus genome in vaccinated rabbits after experimental infection. J. Vet. Med. B. Infect. Dis. Vet. Public Health, 53: 358-362. https://doi.org/10.1111/j.1439-0450.2006.00986.xGall A., Hoffmann B., Teifke J.P., Lange B., Schirrmeier H., 2007. Persistence of viral RNA in rabbits which overcome an experimental RHDV infection detected by a highly sensitive multiplex real-time RT-PCR. Vet. Microbiol.,120: 17-32. https://doi.org/10.1016/j.vetmic.2006.10.006Hall R.N., Mahar J.E., Haboury S., Stevens V., Holmes E.C., Strive T. 2015. Emerging Rabbit Hemorrhagic Disease Virus 2 (RHDVb), Australia. Emerg. Infect. Dis., 21: 2276-2278. https://doi.org/10.3201/eid2112.151210Le Gall G., Boilletot E., Morisse J.P. 1992. Viral haemorrhagic disease of rabbit: purification and characterization of a strain isolated in France. Ann. Rech. Vet., 23: 381-387.Le Gall-ReculĂ© G., Zwingelstein F., Boucher S., Le Normand B., Plassiart G., Portejoie Y., Decors A., Bertagnoli S., GuĂ©rin J.L., Marchandeau S. 2011. Detection of a new variant of rabbit haemorrhagic disease virus in France. Vet. Rec., 168: 137-138. https://doi.org/10.1136/vr.d697Le Gall-ReculĂ© G., Lavazza A., Marchandeau S., Bertagnoli S., Zwingelstein F., Cavadini, P., Martinelli N., Lombardi G., GuĂ©rin J.L., Lemaitre E., Decors A., Boucher S., Le Normand B., Capucci L. 2013. Emergence of a new lagovirus related to Rabbit Haemorrhagic Disease Virus. Vet. Res., 44: 81. https://doi.org/10.1186/1297-9716-44-81Le Gall-ReculĂ© G., Lemaitre E., Bertagnoli S., Hubert C., Top S., Decors A., Marchandeau S., Guitton J.S., 2017. Large-scale lagovirus disease outbreaks in European brown hares (Lepus europaeus) in France caused by RHDV2 strains spatially shared with rabbits (Oryctolagus cuniculus). Vet. Res., 48: 70. https://doi.org/10.1186/s13567-017-0473-yLe Minor O., Beilvert F., Le Moullec T., Djadour D., Martineau J. 2013. Evaluation de l'efficacitĂ© d'un nouveau vaccin contre le virus variant de la maladie hĂ©morragique virale du lapin (VHD).15Ăšmes JournĂ©es de la Recherche Cunicole, 19-20 novembre, Le Mans, France.Le Minor O., Joudou L., Le Moullec T., Beilvert F. 2017. InnocuitĂ© et efficacitĂ© de la vaccination Ă 2 et 3 semaines d'Ăąge contre le virus RHDV2 de la maladie hĂ©morragique virale du lapin (VHD).17Ăšmes JournĂ©es de la Recherche Cunicole, 22-13 novembre, Le Mans, France.Le Pendu J., Abrantes J., Bertagnoli S., Guitton J.S., Le Gall-ReculĂ© G., Lopes A.M., Marchandeau S., Alda F., Almeida T., CĂ©lio A.P., BĂĄrcena J., Burmakina G., Blanco E., Calvete C., Cavadini P., Cooke B., Dalton K., Delibes Mateos M., Deptula W., Eden J.S., Wang F., Ferreira C.C., Ferreira P., Foronda P., Gonçalves D., Gavier-WidĂ©n D., Hall R., Hukowska-Szematowicz B., Kerr P., Kovaliski J., et al. 2017. Proposal for a unified classification system and nomenclature of lagoviruses. J. Gen. Virol., 98:1658-1666. https://doi.org/10.1099/jgv.0.000840Lopes A.M., Correia J., Abrantes J., Melo P., Ramada M., MagalhĂŁes M.J., Alves P.C., Esteves P.J. 2015. Is the new variant RHDV replacing genogroup 1 in Portuguese wild rabbit populations? Viruses, 7: 27-36. https://doi.org/10.3390/v7010027Mahar J.E., Hall R.N., Peacock D., Kovaliski J., Piper M., Mourant R., Huang N., Campbell S., Gu X., Read A., Urakova N., Cox T., Holmes E.C., Strive T. 2018. Rabbit haemorrhagic disease virus 2 (GI.2) is replacing endemic strains of RHDV in the Australian landscape within 18 months of its arrival. J. Virol., https://doi.org/10.1128/JVI.01374-17Martin-Alonso A., Martin-Carrillo N., Garcia-livia K., Valladares B., Foronda P. 2016. Emerging rabbit haemorrhagic disease virus 2 (RHDV2) at the gates of the African continent. Infect. Genet. Evol., 44: 46-50. https://doi.org/10.1016/j.meegid.2016.06.034Morin H., Le Minor O., Beilvert F., Le Moullec T. 2015. DurĂ©e d'immunitĂ© confĂ©rĂ©e par un vaccin vis-Ă -vis des calicivirus classique et variant de la maladie virale hĂ©morragique. 16Ăšmes JournĂ©es de la Recherche Cunicole, 18-19 novembre, Le mans, France.Neimanis A., Larsson Pettersson U., Huang N., GavierâWidĂ©n D.,Strive T. 2018. Elucidation of the pathology and tissue distribution of Lagovirus europaeus GI.2/RHDV2 (rabbit haemorrhagic disease virus 2) in young and adult rabbits (Oryctolagus cuniculus). Vet. Res., 49: 46. https://doi.org/10.1186/s13567-018-0540-zOIE, 2017. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2017. Chapter 2.6.2. Rabbit Haemorrhagic disease. Available at: (Accessed 8 February 2018): http://www.oie.int/fileadmin/Home/fr/Health_standards/tahm/3.06.02_RHD.pdfOIE, 2016. Rabbit Haemorrhagic disease, Canada-immediate notification report. Available at: http://www.oie.int/wahis_2/public/wahid.php/Reviewreport/Review?page_refer=MapFullEventReport&reportid=20799.Puggioni G., Cavadini P., Maestrale C., Scivoli R., Botti G., Ligios C., Le Gall- Recule G., Lavazza A., Capucci L. 2013. The new French 2010 Rabbit Hemorrhagic Disease Virus causes an RHD-like disease in the Sardinian Cape hare (Lepus capensis mediterraneus). Vet. Res., 44: 96.https://doi.org/10.1186/1297-9716-44-96Read A.J., Kirkland P.D. 2017. Efficacy of a commercial vaccine against different strains of rabbit haemorrhagic disease virus. Aust. Vet. J., 95: 223-226. https://doi.org/10.1111/avj.12600SilvĂ©rio D., Lopes A.M., Melo-Ferreira J., MagalhĂŁes M.J., Monterroso P., Serronha A., Maio E., Alves P.C., Esteves P.J., Abrantes J. 2018. Insights into the evolution of the new variant rabbit haemorrhagic disease virus (GI.2) and the identification of novel recombinant strains. Transbound. Emerg. Dis., 65: 983-992. https://doi.org/10.1111/tbed.12830Shien, J.H., Shieh, H.K., Lee, L.H. 2000. Experimental infections of rabbits with rabbit haemorrhagic disease virus monitored by polymerase chain reaction. Res. Vet. Sci., 68, 255-259. https://doi.org/10.1053/rvsc.1999.0372Spikey N., McCabe V.J., Greenwood N.M., Jack S.C., Sutton D., van der Waart L. 2012. Novel bivalent vectored vaccine for control of myxomatosis and rabbit haemorrhagic disease. Vet. Rec., 170: 309. https://doi.org/10.1136/vr.100366Strive T., Wright J., Kovaliski J., Botti G., Capucci L. 2010. The non-pathogenic Australian lagovirus RCV-A1 causes a prolonged infection and elicits partial crossprotection to rabbit haemorrhagic disease virus. Virology, 398, 125-134. https://doi.org/10.1016/j.virol.2009.11.045Westcott D.G., Frossard J.P., Everest D., Dastjerdi A., Duff J.P., Choudhury B. 2014. Incursion of RHDV2- like variant in Great Britain. Vet. Rec., 174: 333-333. https://doi.org/10.1136/vr.g234
The legal framework for financial advertising:curbing behavioural exploitation
Policy makers and behavioural finance scholars express growing concern that marketing practices by financial institutions exploit retail investorsâ behavioural biases. Investor protection regulation should thus address these marketing practices and include mechanisms curbing behavioural exploitation. That raises the question whether the marketing communications regime of the new Markets in Financial Instruments Directive can live up to this demand. This article develops a regulatory model that integrates behavioural finance insights into the new marketing communications regime. It then determines how regulatory authorities can apply this model when they interpret and apply specific regulatory requirements. It demonstrates how a regulatory authority or a court can translate empirical behavioural finance research findings into legal arguments when assessing whether marketing practices can significantly distort a model investorâs decision-making process. The article further establishes that the detailed requirements imposed on investment firms by the new Markets in Financial Instruments Directive are necessary in order to protect investors from behavioural exploitation. Finally, the article submits policy proposals that aim to protect investors more effectively from behavioural exploitation
The 2021 report of the Lancet Countdown on health and climate change: code red for a healthy future
Cost-Effectiveness Analysis of Diagnostic Options for Pneumocystis Pneumonia (PCP)
Diagnosis of Pneumocystis jirovecii pneumonia (PCP) is challenging, particularly in developing countries. Highly sensitive diagnostic methods are costly, while less expensive methods often lack sensitivity or specificity. Cost-effectiveness comparisons of the various diagnostic options have not been presented.We compared cost-effectiveness, as measured by cost per life-years gained and proportion of patients successfully diagnosed and treated, of 33 PCP diagnostic options, involving combinations of specimen collection methods [oral washes, induced and expectorated sputum, and bronchoalveolar lavage (BAL)] and laboratory diagnostic procedures [various staining procedures or polymerase chain reactions (PCR)], or clinical diagnosis with chest x-ray alone. Our analyses were conducted from the perspective of the government payer among ambulatory, HIV-infected patients with symptoms of pneumonia presenting to HIV clinics and hospitals in South Africa. Costing data were obtained from the National Institutes of Communicable Diseases in South Africa. At 50% disease prevalence, diagnostic procedures involving expectorated sputum with any PCR method, or induced sputum with nested or real-time PCR, were all highly cost-effective, successfully treating 77-90% of patients at 189-232 per life-year gained. A relatively cost-effective diagnostic procedure that did not require PCR was Toluidine Blue O staining of induced sputum (109 per life-year gained) compared with several molecular diagnostic options.For diagnosis of PCP, use of PCR technologies, when combined with less-invasive patient specimens such as expectorated or induced sputum, represent more cost-effective options than any diagnostic procedure using BAL, or chest x-ray alone
Potassium and Sodium Transport in Yeast
[EN] As the proper maintenance of intracellular potassium and sodium concentrations
is vital for cell growth, all living organisms have developed a cohort
of strategies to maintain proper monovalent cation homeostasis. In the model yeast
Saccharomyces cerevisiae, potassium is accumulated to relatively high concentrations
and is required for many aspects of cellular function, whereas high intracellular
sodium/potassium ratios are detrimental to cell growth and survival. The fact that
S. cerevisiae cells can grow in the presence of a broad range of concentrations of
external potassium (10 Mâ2.5 M) and sodium (up to 1.5 M) indicates the existence
of robust mechanisms that have evolved to maintain intracellular concentrations of
these cations within appropriate limits. In this review, current knowledge regarding
potassium and sodium transporters and their regulation will be summarized. The
cellular responses to high sodium and potassium and potassium starvation will also
be discussed, as well as applications of this knowledge to diverse fields, including
antifungal treatments, bioethanol production and human disease.L.Y. is funded by grant BFU2011-30197-C03-03 from the Spanish Ministry of Science and Innovation (Madrid, Spain) and EUI2009-04147 [Systems Biology of Microorganisms (SysMo2) European Research Area-Network (ERA-NET)].Yenush, L. (2016). Potassium and Sodium Transport in Yeast. Advances in Experimental Medicine and Biology. 892:187-228. https://doi.org/10.1007/978-3-319-25304-6_8S187228892Ahmed A, Sesti F, Ilan N, Shih TM, Sturley SL et al (1999) A molecular target for viral killer toxin: TOK1 potassium channels. Cell 99:283â291Albert A, Yenush L, Gil-Mascarell MR, Rodriguez PL, Patel S et al (2000) X-ray structure of yeast Hal2p, a major target of lithium and sodium toxicity, and identification of framework interactions determining cation sensitivity. 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Global urban environmental change drives adaptation in white clover.
Urbanization transforms environments in ways that alter biological evolution. We examined whether urban environmental change drives parallel evolution by sampling 110,019 white clover plants from 6169 populations in 160 cities globally. Plants were assayed for a Mendelian antiherbivore defense that also affects tolerance to abiotic stressors. Urban-rural gradients were associated with the evolution of clines in defense in 47% of cities throughout the world. Variation in the strength of clines was explained by environmental changes in drought stress and vegetation cover that varied among cities. Sequencing 2074 genomes from 26 cities revealed that the evolution of urban-rural clines was best explained by adaptive evolution, but the degree of parallel adaptation varied among cities. Our results demonstrate that urbanization leads to adaptation at a global scale
Salmonella bongori provides insights into the evolution of the Salmonellae.
The genus Salmonella contains two species, S. bongori and S. enterica. Compared to the well-studied S. enterica there is a marked lack of information regarding the genetic makeup and diversity of S. bongori. S. bongori has been found predominantly associated with cold-blooded animals, but it can infect humans. To define the phylogeny of this species, and compare it to S. enterica, we have sequenced 28 isolates representing most of the known diversity of S. bongori. This cross-species analysis allowed us to confidently differentiate ancestral functions from those acquired following speciation, which include both metabolic and virulence-associated capacities. We show that, although S. bongori inherited a basic set of Salmonella common virulence functions, it has subsequently elaborated on this in a different direction to S. enterica. It is an established feature of S. enterica evolution that the acquisition of the type III secretion systems (T3SS-1 and T3SS-2) has been followed by the sequential acquisition of genes encoding secreted targets, termed effectors proteins. We show that this is also true of S. bongori, which has acquired an array of novel effector proteins (sboA-L). All but two of these effectors have no significant S. enterica homologues and instead are highly similar to those found in enteropathogenic Escherichia coli (EPEC). Remarkably, SboH is found to be a chimeric effector protein, encoded by a fusion of the T3SS-1 effector gene sopA and a gene highly similar to the EPEC effector nleH from enteropathogenic E. coli. We demonstrate that representatives of these new effectors are translocated and that SboH, similarly to NleH, blocks intrinsic apoptotic pathways while being targeted to the mitochondria by the SopA part of the fusion. This work suggests that S. bongori has inherited the ancestral Salmonella virulence gene set, but has adapted by incorporating virulence determinants that resemble those employed by EPEC.We thank the core sequencing and informatics teams at the Sanger Institute for their assistance and The Wellcome Trust for its support of the Sanger Institute Pathogen Genomics and Biology groups and the MRC for their support of GF, KSR and GNS. MCF, GCL, TRC, HSS, GSV, MS, NKP, RAK, JP, GD and NRT were supported by Wellcome Trust grant 076964 and MICROME, an EU Framework Programme 7 Collaborative Project, Grant Agreement Number 222886-2. Work was also supported by Grant ADI-08/2006 from ComisiĂłn Nacional de InvestigaciĂłn CientĂfica y TecnolĂłgica (CONICYT) and The World Bank, and grant 1100092 from Fondo Nacional de Desarrollo CientĂfico y TecnolĂłgico (FONDECYT). CJB was supported by fellowships from CONICYT (21080373 and AT-24091015)
Salmonelose humana e animal em Araraquara, S. Paulo: prevalĂȘncia de Shigella em casos humanos
Pneumocystis jirovecii pneumonia in tropical and low and middle income countries: a systematic review and meta-regression
Objective: Pneumocystis jirovecii pneumonia (PCP), the commonest opportunistic infection in HIV-infected patients in the developed world, is less commonly described in tropical and low and middle income countries (LMIC). We sought to investigate predictors of PCP in these settings. Design Systematic review and meta-regression. METHODS: Meta-regression of predictors of PCP diagnosis (33 studies). Qualitative and quantitative assessment of recorded CD4 counts, receipt of prophylaxis and antiretrovirals, sensitivity and specificity of clinical signs and symptoms for PCP, co-infection with other pathogens, and case fatality (117 studies). RESULTS: The most significant predictor of PCP was per capita Gross Domestic Product, which showed strong linear association with odds of PCP diagnosis (p30%; treatment was largely appropriate. Prophylaxis appeared to reduce the risk for development of PCP, however 24% of children with PCP were receiving prophylaxis. CD4 counts at presentation with PCP were usually <200Ă10 3/ ml. CONCLUSIONS: There is a positive relationship between GDP and risk of PCP diagnosis. Although failure to diagnose infection in poorer countries may contribute to this, we also hypothesise that poverty exposes at-risk patients to a wide range of infections and that the relatively non-pathogenic P. jirovecii is therefore under-represented. As LMIC develop economically they eliminate the conditions underlying transmission of virulent infection: P. jirovecii , ubiquitous in all settings, then becomes a greater relative threat
Global urban environmental change drives adaptation in white clover
Urbanization transforms environments in ways that alter biological evolution. We examined whether urban environmental change drives parallel evolution by sampling 110,019 white clover plants from 6169 populations in 160 cities globally. Plants were assayed for a Mendelian antiherbivore defense that also affects tolerance to abiotic stressors. Urban-rural gradients were associated with the evolution of clines in defense in 47% of cities throughout the world. Variation in the strength of clines was explained by environmental changes in drought stress and vegetation cover that varied among cities. Sequencing 2074 genomes from 26 cities revealed that the evolution of urban-rural clines was best explained by adaptive evolution, but the degree of parallel adaptation varied among cities. Our results demonstrate that urbanization leads to adaptation at a global scale
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