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Rift Valley Fever for Host Innate Immunity in Resistance to a New A New Mouse Model Reveals a Critical Role for Host Innate Immunity in Resistance to Rift Valley Fever This information is current as Tânia Zaverucha do Valle, Agnès Billecocq, Laurent of September 25, 2021. Guillemot, Rudi Alberts, Céline Gommet, Robert Geffers, Kátia Calabrese, Klaus Schughart, Michèle Bouloy, Xavier Montagutelli and Jean-Jacques Panthier J Immunol 2010; 185:6146-6156; Prepublished online 11 October 2010; Downloaded from doi: 10.4049/jimmunol.1000949 http://www.jimmunol.org/content/185/10/6146 Supplementary http://www.jimmunol.org/content/suppl/2010/10/12/jimmunol.100094 http://www.jimmunol.org/ Material 9.DC1 References This article cites 46 articles, 17 of which you can access for free at: http://www.jimmunol.org/content/185/10/6146.full#ref-list-1 Why The JI? Submit online. by guest on September 25, 2021 • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2010 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology A New Mouse Model Reveals a Critical Role for Host Innate Immunity in Resistance to Rift Valley Fever Taˆnia Zaverucha do Valle,*,† Agne`s Billecocq,‡ Laurent Guillemot,*,† Rudi Alberts,x,{ Ce´line Gommet,‖ Robert Geffers,# Ka´tia Calabrese,** Klaus Schughart,x,{ Miche`le Bouloy,‡ Xavier Montagutelli,*,† and Jean-Jacques Panthier*,† Rift Valley fever (RVF) is an arthropod-borne viral disease repeatedly reported in many African countries and, more recently, in Saudi Arabia and Yemen. RVF virus (RVFV) primarily infects domesticated ruminants, resulting in miscarriage in pregnant females and death for newborns and young animals. It also has the ability to infect humans, causing a feverish syndrome, meningoencephalitis, or hemorrhagic fever. The various outcomes of RVFV infection in animals and humans argue for the existence of host genetic determinants controlling the disease. We investigated the susceptibility of inbred mouse strains to infection with the virulent RVFV ZH548 strain. Compared with classical BALB/cByJ mice, wild-derived Mus m. musculus Downloaded from MBT/Pas mice exhibited earlier and greater viremia and died sooner, a result in sharp contrast with their resistance to infection with West Nile virus and influenza A. Infection of mouse embryonic fibroblasts (MEFs) from MBT/Pas mice with RVFV also resulted in higher viral production. Microarray and quantitative RT-PCR experiments showed that BALB/cByJ MEFs displayed a significant activation of the type I IFN pathway. In contrast, MBT/Pas MEFs elicited a delayed and partial type I IFN response to RVFV infection. RNA interference-mediated inhibition of genes that were not induced by RVFV in MBT/Pas MEFs increased viral production in BALB/cByJ MEFs, thus demonstrating their functional importance in limiting viral replication. We conclude http://www.jimmunol.org/ that the failure of MBT/Pas murine strain to induce, in due course, a complete innate immune response is instrumental in the selective susceptibility to RVF. The Journal of Immunology, 2010, 185: 6146–6156. ift Valley fever (RVF) is an arthropod-borne disease mosquitoes of the genera Aedes and Culex, although other arthro- caused by a virus of the Bunyaviridae family, genus pods may play a role in its spread (1). In natural ecosystems, RVF R Phlebovirus. RVF virus (RVFV) is transmitted mostly by affects mainly sheep, cattle, goats, and humans, but other mammals, such as camels and buffaloes, may exhibit the disease. RVF out- breaks represent a threat for humans in endemic areas, where by guest on September 25, 2021 *Unite´ Ge´ne´tique Fonctionnelle de la Souris, ‡Unite´ Ge´ne´tique Mole´culaire des people may be infected by mosquitoes or by direct contact with ‖ Bunyavirus, and Animalerie Centrale, Institut Pasteur; †Unite´ de Recherche Asso- animals or possibly raw milk (1, 2). They inflict severe economic cie´e 2578, Centre National de la Recherche Scientifique, Paris, France; xDepartment of Infection Genetics, Helmholtz Centre for Infection Research, Braunschweig; losses, especially upon trade activities (1). Originally present in {University of Veterinary Medicine, Hannover; #Department of Cell Biology, Ar- Eastern and Southern Africa, RVFV has spread in recent years to ray Facility, Helmholtz Centre for Infection Research, Braunschweig, Germany Western Africa, Madagascar, and even outside Africa to Saudi **Fundac¸a˜o Oswaldo Cruz, Laborato´rio de Imunomodulac¸a˜o e Protozoologia, Rio de Janeiro, Brazil Arabia and Yemen (3). Received for publication March 25, 2010. Accepted for publication September 8, The RVFV has a tripartite ssRNA genome, consisting of large, 2010. medium, and small segments. The small segment encodes the N This work was supported in part by “ResistFever” Grant 07-GANI-007 from the nucleocapsid and the small segment nonstructural protein (NSs) (4), Agence Nationale de la Recherche. It was also supported by a Programme Trans- which is a main factor of virulence. Indeed, the deletion of NSs is versal de Recherche grant awarded to K.S., M.B., and J.-J.P. from the Helmholtz Centre for Infection Research and the Institut Pasteur. Part of this work was facili- responsible for RVFV avirulence in mice (5). NSs protein acts tated through the International Network for Capacity Building for the Control of through several independent mechanisms. Early postinfection (p.i.), Emerging Viral Vector Borne Zoonotic Diseases (Arbo-Zoonet) supported by the NSs interacts with Sin3A associated protein 30, a subunit of histone European Union under Grant Agreement 211757 and the Arbo-Zoonet Coordination Action Project 211757 of the European Commission. The Unite´ Fonctionnelle de la deacetylase complex, and maintains the promoter of IFN-b (Ifnb1) Souris at the Institut Pasteur is supported by Merck Serono. T.Z.V. was awarded gene in a transcriptionally silent state, blocking the production of fellowships from Conselho Nacional de Desenvolvimento Cientifico e Technologico, Brazil (210215/2006-2) and the Agence Nationale de la Recherche. R.A. is supported IFN-b as early as 3–4 h p.i. (6). NSs also induces the specific de- by the Helmholtz Virtual Centre “GeNeSys–German Network for Systems Genetics.” gradation of the dsRNA-dependent protein kinase PKR/EIF2AK2 The microarray data presented in this article have been submitted to the National and facilitates efficient viral translation (7, 8). Moreover, NSs se- Center for Biotechnology Information’s Gene Expression Omnibus under accession questers p44 and XPB, subunits of the RNA polymerase II TFIIH number GSE18064. factor. This sequestration was correlated with the general inhibition Address correspondence and reprint requests to Prof. J.-J. Panthier and Prof. M. of cellular transcription in RVFV-infected cells, which occurs at Bouloy, Institut Pasteur, 25 Rue du Docteur Roux, 75724 Paris Cedex, France. E-mail addresses: [email protected] and [email protected] late stages of infection (.8–9 h p.i) (9). The online version of this article contains supplemental material. Genetic determinants seem to play an important role in modeling Abbreviations used in this paper: ISG, IFN-stimulated gene; MEF, mouse embryonic RVF outcomes. In humans, infection may lead to a great variety of fibroblast; MOI, multiplicity of infection; NS, small segment nonstructural protein; clinical manifestations that range from a febrile influenza-like ill- p.i., postinfection; qRT-PCR, quantitative RT-PCR; RVF, Rift Valley fever; RVFV, ness to retinitis, encephalitis, and hepatitis with fatal hemorrhagic Rift Valley fever virus; siRNA, small interfering RNA. fever (1). Similarly, a wide variation in susceptibility to RVF is Copyright Ó 2010 by The American Association of Immunologists, Inc. 0022-1767/10/$16.00 observed in different animal breeds, ranging from unapparent or www.jimmunol.org/cgi/doi/10.4049/jimmunol.1000949 The Journal of Immunology 6147 moderate febrile reactions to high fevers, severe prostration, and Materials and Methods death in the most susceptible animals (2). Experiments with the rat Ethics statement model confirmed the existence of genetic determinants in RVF (10– All studies on animals followed the guidelines on the ethical use of animals 13). However, surprisingly, an influence of genetic factors could not from the European Communities Council Directive of November 24, 1986 be demonstrated in a large survey of 34 classical inbred laboratory (86/609/EEC). All animal experiments were approved and conducted in mouse strains (11). To further decipher the host–pathogen in- accordance with the Institut Pasteur Biosafety Committee. teraction in mice, we tested the susceptibility of additional inbred Mice, cells, and virus strains of mice by including mouse strains derived from mice of various Mus subspecies recently trapped in the wild. This collection BALB/cByJ and C57BL/6J inbred mice were purchased from Charles
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