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dc.contributor.authorSebayang, A.A.
dc.contributor.authorFahlena, H.
dc.contributor.authorAnam, V. 
dc.contributor.authorKnopoff, D.A. 
dc.contributor.authorStollenwerk, N. 
dc.contributor.authorAguiar, M. 
dc.contributor.authorSoewono, E.
dc.date.accessioned2021-10-14T19:04:40Z
dc.date.available2021-10-14T19:04:40Z
dc.date.issued2021-09-01
dc.identifier.issn2079-7737
dc.identifier.urihttp://hdl.handle.net/20.500.11824/1351
dc.description.abstractDengue fever is a viral mosquito-borne infection and a major international public health concern. With 2.5 billion people at risk of acquiring the infection around the world, disease severity is influenced by the immunological status of the individual, seronegative or seropositive, prior to natural infection. Caused by four antigenically related but distinct serotypes, DENV-1 to DENV-4, infection by one serotype confers life-long immunity to that serotype and a period of temporary cross-immunity (TCI) to other serotypes. The clinical response on exposure to a second serotype is complex with the so-called antibody-dependent enhancement (ADE) process, a disease augmentation phenomenon when pre-existing antibodies to previous dengue infection do not neutralize but rather enhance the new infection, used to explain the etiology of severe disease. In this paper, we present a minimalistic mathematical model framework developed to describe qualitatively the dengue immunological response mediated by antibodies. Three models are analyzed and compared: (i) primary dengue infection, (ii) secondary dengue infection with the same (homologous) dengue virus and (iii) secondary dengue infection with a different (heterologous) dengue virus. We explore the features of viral replication, antibody production and infection clearance over time. The model is developed based on body cells and free virus interactions resulting in infected cells activating antibody production. Our mathematical results are qualitatively similar to the ones described in the empiric immunology literature, providing insights into the immunopathogenesis of severe disease. Results presented here are of use for future research directions to evaluate the impact of dengue vaccines.en_US
dc.description.sponsorshipA.S, H.F., and E.S. E.S. has received funded from the Indonesian RistekBrin Grant No. 122M/IT1.C02/TA.00/2021, 2021 (previously RistekDikti 2018-2021). M.A. received funding from the European Union’s Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement No 792494.en_US
dc.formatapplication/pdfen_US
dc.language.isoengen_US
dc.rightsReconocimiento-NoComercial-CompartirIgual 3.0 Españaen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/es/en_US
dc.subjectAntibodiesen_US
dc.subjectAntibody-dependent enhancementen_US
dc.subjectDengue feveren_US
dc.subjectImmune responseen_US
dc.subjectViral loaden_US
dc.subjectWithin-host modelingen_US
dc.titleModeling dengue immune responses mediated by antibodies: A qualitative studyen_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.identifier.doi10.3390/biology10090941en_US
dc.relation.publisherversionhttps://www.mdpi.com/2079-7737/10/9/941en_US
dc.relation.projectIDES/1PE/SEV-2017-0718en_US
dc.relation.projectIDEUS/BERC/BERC.2018-2021en_US
dc.relation.projectIDEUS/BMTFen_US
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessen_US
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersionen_US
dc.journal.titleBiologyen_US
dc.volume.number10en_US
dc.issue.number9en_US


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Reconocimiento-NoComercial-CompartirIgual 3.0 España
Except where otherwise noted, this item's license is described as Reconocimiento-NoComercial-CompartirIgual 3.0 España