Journal
CELL HOST & MICROBE
Volume 2, Issue 6, Pages 417-426Publisher
CELL PRESS
DOI: 10.1016/j.chom.2007.09.015
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Funding
- Intramural NIH HHS Funding Source: Medline
- NIAID NIH HHS [AI061373, U54 AI057160-010003, U01 AI061373, U54 AI057160, U01 AI061373-03] Funding Source: Medline
- PHS HHS [HHSN266200600013C] Funding Source: Medline
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Severe dengue virus infection can occur in humans with pre-existing antibodies against the virus. This observation led to the hypothesis that a subneutralizing antibody level in vivo can increase viral burden and cause more severe disease. Indeed, antibody-dependent enhancement of infection (ADE) in vitro has been described for multiple viruses, including the flaviviruses dengue virus and West Nile virus. Here, we demonstrate that the complement component C1q restricts ADE by anti-flavivirus IgG antibodies in an IgG subclass-specific manner in cell culture and in mice. IgG subclasses that avidly bind C1q induced minimal ADE in the presence of C1q. These findings add a layer of complexity for the analysis of humoral immunity and flavivirus infection.
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