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Immunol Rev. 2015 Nov;268(1):340-64. doi: 10.1111/imr.12367.

Fc receptors in antibody-dependent enhancement of viral infections.

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Emerging Viruses and Inflammation Research Group, Institute for Glycomics, Griffith University, Gold Coast, Qld, Australia.
HKU-Pasteur Research Pole, School of Public Health, The University of Hong Kong, Hong Kong SAR, Hong Kong.
Department of Cell Biology and Infection, Institut Pasteur, Paris, France.
Discipline of Pathology, Bosch Institute, School of Medical Sciences, Sydney Medical School, Charles Perkins Centre, University of Sydney, Sydney, NSW, Australia.


Sensitization of the humoral immune response to invading viruses and production of antiviral antibodies forms part of the host antiviral repertoire. Paradoxically, for a number of viral pathogens, under certain conditions, antibodies provide an attractive means of enhanced virus entry and replication in a number of cell types. Known as antibody-dependent enhancement (ADE) of infection, the phenomenon occurs when virus-antibody immunocomplexes interact with cells bearing complement or Fc receptors, promoting internalization of the virus and increasing infection. Frequently associated with exacerbation of viral disease, ADE of infection presents a major obstacle to the prevention of viral disease by vaccination and is thought to be partly responsible for the adverse effects of novel antiviral therapeutics such as intravenous immunoglobulins. There is a growing body of work examining the intracellular signaling pathways and epitopes responsible for mediating ADE, with a view to aiding rational design of antiviral strategies. With in vitro studies also confirming ADE as a feature of infection for a growing number of viruses, challenges remain in understanding the multilayered molecular mechanisms of ADE and its effect on viral pathogenesis.


Fc receptors; antibody-dependent enhancement; intravenous immunoglobulins; virus

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