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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 Barré 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.

Original publication

DOI

10.1038/ni.3515

Type

Journal article

Journal

Nature immunology

Publication Date

09/2016

Volume

17

Pages

1102 - 1108

Addresses

Division of Immunology and Inflammation, Department of Medicine, Hammersmith Campus, Imperial College London, UK.

Keywords

Cells, Cultured, Humans, Dengue Virus, Dengue, Microcephaly, Guillain-Barre Syndrome, Viral Envelope Proteins, Antibodies, Monoclonal, Antibodies, Viral, Immunodominant Epitopes, Epitope Mapping, Antibody-Dependent Enhancement, Virus Replication, Cross Reactions, Protein Binding, Adolescent, Child, Child, Preschool, South America, Female, Male, Antibodies, Neutralizing, Zika Virus, Zika Virus Infection