Journal
NATURE IMMUNOLOGY
Volume 17, Issue 9, Pages 1102-1108Publisher
NATURE PORTFOLIO
DOI: 10.1038/ni.3515
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Funding
- Medical Research Council, UK
- Wellcome Trust, UK
- National Institute for Health Research Biomedical Research Centre
- European Commission [282 378]
- Laboratory of Excellence Integrative Biology of Emerging Infectious Diseases [ANR-10-LABX-62-IBEID]
- Agence Nationale de la Recherche [FlaviStem/I1378]
- Thailand Research Fund through the Royal Golden Jubilee PhD
- MRC [G0400720, G0801508] Funding Source: UKRI
- Medical Research Council [MR/N012658/1, G0801508, G0600000, G0400720] Funding Source: researchfish
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Zika virus (ZIKV) was discovered in 1947 and was thought to lead to relatively mild disease. The recent explosive outbreak of ZIKV in South America has led to widespread concern, with reports of neurological sequelae ranging from Guillain Barre syndrome to microcephaly. ZIKV infection has occurred in areas previously exposed to dengue virus (DENV), a flavivirus closely related to ZIKV. Here we investigated the serological cross-reaction between the two viruses. Plasma immune to DENV showed substantial cross-reaction to ZIKV and was able to drive antibody-dependent enhancement (ADE) of ZIKV infection. Using a panel of human monoclonal antibodies (mAbs) to DENV, we showed that most antibodies that reacted to DENV envelope protein also reacted to ZIKV. Antibodies to linear epitopes, including the immunodominant fusion-loop epitope, were able to bind ZIKV but were unable to neutralize the virus and instead promoted ADE. Our data indicate that immunity to DENV might drive greater ZIKV replication and have clear implications for disease pathogenesis and future vaccine programs for ZIKV and DENV.
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