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PLoS One. 2018 Jul 25;13(7):e0200478. doi: 10.1371/journal.pone.0200478. eCollection 2018.

Dengue immune sera enhance Zika virus infection in human peripheral blood monocytes through Fc gamma receptors.

Author information

1
CAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences (CAS), Shanghai, China.
2
University of Chinese Academy of Sciences, Beijing, China.
3
Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
4
School of Life Sciences, Shanghai University, Shanghai, China.

Abstract

Antibody dependent enhancement (ADE) has most often been associated with dengue virus (DENV). Studies using leukemia cell lines suggest that DENV specific antibodies can enhance Zika virus (ZIKV) infectivity, and vice versa. To examine the mechanisms of ADE of ZIKV infection in primary human cells, we assessed 40 serum samples obtained from convalescent DENV-1 or DENV-3 infected subjects. All sera tested exhibited high binding potency, while modest or none neutralization activities against ZIKV. Primary CD14+ monocytes, rather than B and T cells in peripheral blood mononuclear cells (PBMCs), were found to be the mediators of the enhancement of ZIKV infectivity by DENV immune sera. Monocyte-derived immature dendritic cells (DCs), but not mature DCs were highly permissive to ZIKV infection, whereas neither immature nor mature DCs could mediate enhanced ZIKV infection in the presence of DENV immune sera. In addition, antibody blocking of either FcγRI (CD64), or FcγRII (CD32), or FcγRIII (CD16) resulted in diminished ADE of ZIKV infection. Our findings provide an improved understanding of the pathogenesis of ZIKV infection, and inform rational vaccine design.

PMID:
30044839
PMCID:
PMC6059439
DOI:
10.1371/journal.pone.0200478
[Indexed for MEDLINE]
Free PMC Article

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