Show simple item record

dc.contributor.authorMatar, Caline G
dc.contributor.authorAnthony, Neil R
dc.contributor.authorO'Flaherty, Brigid M
dc.contributor.authorJacobs, Nathan T
dc.contributor.authorPriyamvada, Lalita
dc.contributor.authorEngwerda, Christian R
dc.contributor.authorSpeck, Samuel H
dc.contributor.authorLamb, Tracey J
dc.date.accessioned2021-05-06T04:39:07Z
dc.date.available2021-05-06T04:39:07Z
dc.date.issued2015
dc.identifier.issn1553-7366
dc.identifier.doi10.1371/journal.ppat.1004858
dc.identifier.urihttp://hdl.handle.net/10072/404199
dc.description.abstractImmunity to non-cerebral severe malaria is estimated to occur within 1-2 infections in areas of endemic transmission for Plasmodium falciparum. Yet, nearly 20% of infected children die annually as a result of severe malaria. Multiple risk factors are postulated to exacerbate malarial disease, one being co-infections with other pathogens. Children living in Sub-Saharan Africa are seropositive for Epstein Barr Virus (EBV) by the age of 6 months. This timing overlaps with the waning of protective maternal antibodies and susceptibility to primary Plasmodium infection. However, the impact of acute EBV infection on the generation of anti-malarial immunity is unknown. Using well established mouse models of infection, we show here that acute, but not latent murine gammaherpesvirus 68 (MHV68) infection suppresses the anti-malarial humoral response to a secondary malaria infection. Importantly, this resulted in the transformation of a non-lethal P. yoelii XNL infection into a lethal one; an outcome that is correlated with a defect in the maintenance of germinal center B cells and T follicular helper (Tfh) cells in the spleen. Furthermore, we have identified the MHV68 M2 protein as an important virus encoded protein that can: (i) suppress anti-MHV68 humoral responses during acute MHV68 infection; and (ii) plays a critical role in the observed suppression of anti-malarial humoral responses in the setting of co-infection. Notably, co-infection with an M2-null mutant MHV68 eliminates lethality of P. yoelii XNL. Collectively, our data demonstrates that an acute gammaherpesvirus infection can negatively impact the development of an anti-malarial immune response. This suggests that acute infection with EBV should be investigated as a risk factor for non-cerebral severe malaria in young children living in areas endemic for Plasmodium transmission.
dc.description.peerreviewedYes
dc.languageEnglish
dc.publisherPublic Library Science
dc.relation.ispartofpagefrom1
dc.relation.ispartofpageto23
dc.relation.ispartofissue5
dc.relation.ispartofjournalPLOS Pathogens
dc.relation.ispartofvolume11
dc.subject.fieldofresearchMicrobiology
dc.subject.fieldofresearchImmunology
dc.subject.fieldofresearchMedical microbiology
dc.subject.fieldofresearchcode3107
dc.subject.fieldofresearchcode3204
dc.subject.fieldofresearchcode3207
dc.subject.keywordsScience & Technology
dc.subject.keywordsLife Sciences & Biomedicine
dc.subject.keywordsMicrobiology
dc.subject.keywordsParasitology
dc.subject.keywordsVirology
dc.titleGammaherpesvirus Co-infection with Malaria Suppresses Anti-parasitic Humoral Immunity
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationMatar, CG; Anthony, NR; O'Flaherty, BM; Jacobs, NT; Priyamvada, L; Engwerda, CR; Speck, SH; Lamb, TJ, Gammaherpesvirus Co-infection with Malaria Suppresses Anti-parasitic Humoral Immunity, PLOS PATHOGENS, 2015, 11 (5)
dcterms.dateAccepted2015-04-06
dcterms.licensehttps://creativecommons.org/licenses/by/4.0/
dc.date.updated2021-05-06T04:34:04Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2015 Matar et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
gro.hasfulltextFull Text
gro.griffith.authorEngwerda, Christian R.


Files in this item

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record