期刊
CELL HOST & MICROBE
卷 6, 期 4, 页码 381-391出版社
CELL PRESS
DOI: 10.1016/j.chom.2009.09.003
关键词
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资金
- Intramural Research Program of the National Institutes of Allergy and Infectious Diseases (NIAID)
- Pediatric Dengue Vaccine Initiative
- National Institutes of Health (NIH) [U01 A1061373, R01 A1073755]
- Midwest Regional Center of Excellence for Biodefense and Emerging Infectious Diseases Research [U54 AI057160]
Virus neutralization is governed by the number of antibodies that bind a virion during the cellular entry process. Cellular and serum factors that interact with antibodies have the potential to modulate neutralization potency. Although the addition of serum complement can increase the neutralizing activity of antiviral antibodies in vitro, the mechanism and significance of this augmented potency in vivo remain uncertain. Herein, we show that the complement component C1q increases the potency of antibodies against West Nile virus by modulating the stoichiometric requirements for neutralization. The addition of C1q does not result in virolysis but instead reduces the number of antibodies that must bind the virion to neutralize infectivity. For IgG subclasses that bind C1q avidly, this reduced stoichiometric threshold falls below the minimal number of antibodies required for antibody-dependent enhancement (ADE) of infection of cells expressing Fc-gamma receptors (CD32) and explains how C1q restricts the ADE of flavivirus infection.
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