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Antibody-dependent enhancement (ADE) of infection is a phenomenon observed during secondary infection caused by some viruses (primarily, from the Flaviviridae family), including dengue virus (DENV), Zika virus (ZIKV), West Nile virus (WNV), tick-borne encephalitis virus, yellow fever virus, and some others. There are two types of ADE mediated by (i) Fc receptors and (ii) receptors for complement system components. The first type involves 4 types of Fc receptors for IgG molecules (FcRI, FcRIIa, FcRIIb, and FcRIIIa) which ensure the binding of the virus-antibody complex to the target cell and its subsequent internalization. The Fc-mediated uptake of the virus is an active process that involves a number of signaling molecules and triggers branched cascades of activation events. The Fc-mediated pathway of viral entry increases the viral load and switches the cell from the antiviral response to the proinflammatory pathway, thus promoting more efficient viral replication. Unlike other Fc receptors, FcRIIb bound to IgG inhibits the capture of the virus-antibody complex and prevents the ADE. The development of ADE in response to vaccination is highly undesirable. Understanding the biochemical mechanisms underlying ADE is important for the development of new vaccines and therapeutic monoclonal antibodies for protecting against viral infections.
Filatov et al. (Thu,) studied this question.