期刊
CELL REPORTS
卷 25, 期 6, 页码 1385-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.10.031
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类别
资金
- US Department of Energy
- NIH (NIGMS)
- NIH (National Cancer Institute)
- NIH [1R21AI129479-01, U19AI111825, UL1TR001866, R01AI037526, UM1AI100663, P01AI138938, R01AI124690, U19AI057229]
- Lyda Hill
- Rockefeller University Development Office
- Office of Research Infrastructure Programs/OD [P51OD011107]
- Pathology, Microbiology and Immunology Department
- Molecular Observatory at Caltech
- Gordon and Betty Moore Foundation
- Robertson Therapeutic Development Fund
- Pew Latin American Fellows Program in the Biomedical Sciences
- Studienstiftung des deutschen Volkes
Zika virus (ZIKV) causes severe neurologic complications and fetal aberrations. Vaccine development is hindered by potential safety concerns due to antibody cross-reactivity with dengue virus and the possibility of disease enhancement. In contrast, passive administration of anti-ZIKV antibodies engineered to prevent enhancement may be safe and effective. Here, we report on human monoclonal antibody Z021, a potent neutralizer that recognizes an epitope on the lateral ridge of the envelope domain III (EDIII) of ZIKV and is protective against ZIKV in mice. When administered to macaques undergoing a high-dose ZIKV challenge, a single anti-EDIII antibody selected for resistant variants. Co-administration of two antibodies, Z004 and Z021, which target distinct sites on EDIII, was associated with a delay and a 3-to 4-log decrease in peak viremia. Moreover, the combination of these antibodies engineered to avoid enhancement prevented viral escape due to mutation in macaques, a natural host for ZIKV.
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