Publication: Dengue virus sero-cross-reactivity drives antibody-dependent enhancement of infection with zika virus
Issued Date
2016-08-19
Resource Type
ISSN
15292916
15292908
15292908
DOI
Other identifier(s)
2-s2.0-84976292755
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Nature Immunology. Vol.17, No.9 (2016), 1102-1108
Suggested Citation
Wanwisa Dejnirattisai, Piyada Supasa, Wiyada Wongwiwat, Alexander Rouvinski, Giovanna Barba-Spaeth, Thaneeya Duangchinda, Anavaj Sakuntabhai, Van Mai Cao-Lormeau, Prida Malasit, Felix A. Rey, Juthathip Mongkolsapaya, Gavin R. Screaton Dengue virus sero-cross-reactivity drives antibody-dependent enhancement of infection with zika virus. Nature Immunology. Vol.17, No.9 (2016), 1102-1108. doi:10.1038/ni.3515 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/40765
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Dengue virus sero-cross-reactivity drives antibody-dependent enhancement of infection with zika virus
Abstract
© 2016 Nature America, Inc. 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.