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Updated: May 28, 2026
Quantification of Antibody-dependent Enhancement of the Zika Virus in Primary Human Cells
Published on: January 18, 2019
Antibody-dependent enhancement of Marburg virus infection
Eri Nakayama1, Daisuke Tomabechi, Keita Matsuno
1Department of Global Epidemiology, Hokkaido University Research Center for Zoonosis Control, Sapporo, Japan.
Background:
Marburg virus (MARV) and Ebola virus (EBOV) cause severe hemorrhagic fever in primates. Earlier studies demonstrated that antibodies to particular epitopes on the glycoprotein (GP) of EBOV enhanced virus infectivity in vitro.
Methods:
To investigate this antibody-dependent enhancement (ADE) in MARV infection, we produced mouse antisera and monoclonal antibodies (mAbs) to the GPs of MARV strains Angola and Musoke.
Results:
The infectivity of vesicular stomatitis virus pseudotyped with Angola GP in K562 cells was significantly enhanced in the presence of Angola GP antisera, whereas only minimal ADE activity was seen with Musoke GP antisera. This difference correlated with the percentage of hybridoma clones producing infectivity-enhancing mAbs. Using mAbs to MARV GP, we identified 3 distinct ADE epitopes in the mucinlike region on Angola GP. Interestingly, some of these antibodies bound to both Angola and Musoke GPs but showed significantly higher ADE activity for strain Angola. ADE activity depended on epitopes in the mucinlike region and glycine at amino acid position 547, present in the Angola but absent in the Musoke GP.
Conclusions:
These results suggest a possible link between ADE and MARV pathogenicity and provide new insights into the mechanisms underlying ADE entry of filoviruses.
Insights
Antibody-dependent enhancement (ADE) can increase Marburg virus (MARV) infectivity. Specific epitopes on MARV glycoprotein (GP) drive this ADE, potentially linking to MARV pathogenicity.
Area of Science:
- Virology
- Immunology
Background:
- Marburg virus (MARV) and Ebola virus (EBOV) are filoviruses causing severe hemorrhagic fever in primates.
- Antibodies targeting specific glycoprotein (GP) epitopes on EBOV can enhance viral infectivity (antibody-dependent enhancement - ADE).
Purpose of the Study:
- To investigate antibody-dependent enhancement (ADE) in Marburg virus (MARV) infection.
- To identify specific epitopes on MARV GP responsible for ADE.
Main Methods:
- Produced mouse antisera and monoclonal antibodies (mAbs) against MARV strains Angola and Musoke GPs.
- Assessed ADE activity using pseudotyped vesicular stomatitis virus (VSV) in K562 cells.
- Mapped ADE epitopes on MARV GP using mAbs.
Main Results:
- MARV Angola GP antisera significantly enhanced pseudotyped virus infectivity, while Musoke GP antisera showed minimal ADE.
- Identified three distinct ADE epitopes within the mucin-like region of Angola GP.
- ADE activity was linked to specific epitopes and glycine at amino acid position 547 in Angola GP, absent in Musoke GP.
Conclusions:
- Findings suggest a link between ADE and MARV pathogenicity.
- Provides novel insights into the mechanisms of ADE entry for filoviruses.
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