Abstract
We propose for the first time that antibody–dependent enhancement (ADE) of viral infection has served as an evolutionary selection pressure in which species that produce truncated immunoglobulin–Y (IgY) have had a selective advantage. The absence of the Fc region prevents binding of antibody–covered virions to cellular Fc receptors and to complement component C1q, thus preventing ADE by these mechanisms and limiting viral entry to cells. It logically follows that the range of cell types potentially infected would be reduced, slowing the invasive nature of viral infections. We briefly review the structure, function and evolution of IgY, the mechanisms of ADE, discuss how producing truncated immunoglobulins could limit ADE, and how future research can falsify or confirm this hypothesis.
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