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dc.contributor.authorCamejo, Ana
dc.contributor.authorCordeiro, Cynthia
dc.contributor.authorJulien, Lindsay
dc.contributor.authorGrotenbreg, Gijsbert M.
dc.contributor.authorFrickel, Eva-Maria
dc.contributor.authorYoung, Lucy
dc.contributor.authorPloegh, Hidde
dc.contributor.authorMelo, Mariane Bandeira
dc.contributor.authorSaeij, Jeroen
dc.contributor.authorJensen, Kirk D.
dc.date.accessioned2015-04-02T17:36:19Z
dc.date.available2015-04-02T17:36:19Z
dc.date.issued2015-02
dc.date.submitted2014-11
dc.identifier.issn2150-7511
dc.identifier.urihttp://hdl.handle.net/1721.1/96341
dc.description.abstractThe intracellular parasite Toxoplasma gondii infects a wide variety of vertebrate species globally. Infection in most hosts causes a lifelong chronic infection and generates immunological memory responses that protect the host against new infections. In regions where the organism is endemic, multiple exposures to T. gondii likely occur with great frequency, yet little is known about the interaction between a chronically infected host and the parasite strains from these areas. A widely used model to explore secondary infection entails challenge of chronically infected or vaccinated mice with the highly virulent type I RH strain. Here, we show that although vaccinated or chronically infected C57BL/6 mice are protected against the type I RH strain, they are not protected against challenge with most strains prevalent in South America or another type I strain, GT1. Genetic and genomic analyses implicated the parasite-secreted rhoptry effectors ROP5 and ROP18, which antagonize the host’s gamma interferon-induced immunity-regulated GTPases (IRGs), as primary requirements for virulence during secondary infection. ROP5 and ROP18 promoted parasite superinfection in the brains of challenged survivors. We hypothesize that superinfection may be an important mechanism to generate T. gondii strain diversity, simply because two parasite strains would be present in a single meal consumed by the feline definitive host. Superinfection may drive the genetic diversity of Toxoplasma strains in South America, where most isolates are IRG resistant, compared to North America, where most strains are IRG susceptible and are derived from a few clonal lineages. In summary, ROP5 and ROP18 promote Toxoplasma virulence during reinfection.en_US
dc.language.isoen_US
dc.publisherAmerican Society for Microbiologyen_US
dc.relation.isversionofhttp://dx.doi.org/10.1128/mBio.02280-14en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alikeen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/en_US
dc.sourceAmerican Society for Microbiologyen_US
dc.titleToxoplasma gondii Superinfection and Virulence during Secondary Infection Correlate with the Exact [ROP5 over ROP18] Allelic Combinationen_US
dc.typeArticleen_US
dc.identifier.citationJensen, Kirk D. C., Ana Camejo, Mariane B. Melo, Cynthia Cordeiro, Lindsay Julien, Gijsbert M. Grotenbreg, Eva-Maria Frickel, Hidde L. Ploegh, Lucy Young, and Jeroen P. J. Saeij. “ Toxoplasma Gondii Superinfection and Virulence During Secondary Infection Correlate with the Exact [ROP5 over ROP18] Allelic Combination .” mBio 6, no. 2 (February 24, 2015): e02280–14.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentWhitehead Institute for Biomedical Researchen_US
dc.contributor.departmentKoch Institute for Integrative Cancer Research at MITen_US
dc.contributor.mitauthorPloegh, Hiddeen_US
dc.contributor.mitauthorMelo, Mariane Bandeiraen_US
dc.contributor.mitauthorJensen, Kirk D. C.en_US
dc.contributor.mitauthorCamejo, Anaen_US
dc.contributor.mitauthorSaeij, Jeroenen_US
dc.contributor.mitauthorCordeiro, Cynthiaen_US
dc.contributor.mitauthorJulien, Lindsayen_US
dc.relation.journalmBioen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsJensen, Kirk D. C.; Camejo, Ana; Melo, Mariane B.; Cordeiro, Cynthia; Julien, Lindsay; Grotenbreg, Gijsbert M.; Frickel, Eva-Maria; Ploegh, Hidde L.; Young, Lucy; Saeij, Jeroen P. J.en_US
dc.identifier.orcidhttps://orcid.org/0000-0002-1090-6071
mit.licensePUBLISHER_CCen_US


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