[Source: PLoS One, full page: (LINK). Abstract, edited.]
OPEN ACCESS / PEER-REVIEWED / RESEARCH ARTICLE
DNA-immunisation with dengue virus E protein domains I/II, but not domain III, enhances Zika, West Nile and Yellow Fever virus infection
Jose L. Slon Campos , Monica Poggianella , Sara Marchese, Monica Mossenta, Jyoti Rana, Francesca Arnoldi, Marco Bestagno, Oscar R. Burrone
Published: July 25, 2017 / DOI: https://doi.org/10.1371/journal.pone.0181734
Dengue virus (DENV), the causative agent of dengue disease, is among the most important mosquito-borne pathogens worldwide. DENV is composed of four closely related serotypes and belongs to the Flaviviridae family alongside other important arthropod-borne viral pathogens such as Zika virus (ZIKV), West Nile virus (WNV) and Yellow Fever virus (YFV). After infection, the antibody response is mostly directed to the viral E glycoprotein which is composed of three structural domains named DI, DII and DIII that share variable degrees of homology among different viruses. Recent evidence supports a close serological interaction between ZIKV and DENV. The possibility of worse clinical outcomes as a consequence of antibody-dependent enhancement of infection (ADE) due to cross-reactive antibodies with poor neutralisation activity is a matter of concern. We tested polyclonal sera from groups of female Balb/C mice vaccinated with DNA constructs expressing DI/DII, DIII or the whole sE from different DENV serotypes and compared their activity in terms of cross-reactivity, neutralisation of virus infection and ADE. Our results indicate that the polyclonal antibody responses against the whole sE protein are highly cross-reactive with strong ADE and poor neutralisation activities due to DI/DII immunodominance. Conversely, anti-DIII polyclonal antibodies are type-specific, with no ADE towards ZIKV, WNV and YFV, and strong neutralisation activity restricted only to DENV.
Citation: Slon Campos JL, Poggianella M, Marchese S, Mossenta M, Rana J, Arnoldi F, et al. (2017) DNA-immunisation with dengue virus E protein domains I/II, but not domain III, enhances Zika, West Nile and Yellow Fever virus infection. PLoS ONE 12(7): e0181734. https://doi.org/10.1371/journal.pone.0181734
Editor: Dong-Yan Jin, University of Hong Kong, HONG KONG
Received: March 13, 2017; Accepted: July 6, 2017; Published: July 25, 2017
Copyright: © 2017 Slon Campos 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.
Data Availability: All relevant data are within the paper and its Supporting Information files.
Funding: JLSC and JR were supported by Arturo Falaschi ICGEB pre-doctoral and postdoctoral fellowships, respectively. FA was supported by FIRB-Futuro in Ricerca grant (RBFR13209E), Ministero dell’Istruzione, dell’Università e della Ricerca (MIUR), Italy. The funders played no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: I have read the journal’s policy and the authors of this manuscript have the following competing interests: A patent (Italian patent RM2013A000458 “Antidengue virus genetic vaccine based on the envelope protein ectodomains”) on the invention of the antigen construct for DNA vaccination has been filed by MP, MB, and ORB. This does not alter our adherence to all PLOS policies on sharing data and materials.
Keywords: Dengue Fever; Zika Virus; West Nile Virus; Yellow Fever.