Box 2.
Structure-function considerations in antiviral antibodies that may confer protection*.
| “Fc-independent” Ab-binding is sufficient. Fe serves only half-life and valency | “Fc-dependent” Ab-binding is necessary but insufficient. Fe is required for one or more functions |
|---|---|
| • “Neutralization” i.e., Abs that act solely as antagonists of viral binding, entry, or launch as in many common assays • Aggregation of virions to functionally suppress numbers of infectious units. • Antagonism of viral assembly, e.g., competitive inhibitors of trimmer formations or required cleavages. • Antagonism of viral release processes, e.g., anti-neuraminidase • Antagonism of viral “virulence factors” that otherwise exacerbate disease, promote intercellular spread, or aid transmission |
Opsonization: Abs that exploit FeR to redirect infectious virions to insusceptible cells, e.g., neutrophils. • Cell-targeting antibodies (CTAb) that require Fe receptor (FeR) interaction for manifestation of antiviral effect. - ADCC as measured (17) for example by: direct lysis of infected cells; trogocytosis (RFADCC); phagocytosis; granzyme release/signaling by NK - Complement activation: lytic cascade; other pleotropic effects of partial complement activation • many other potential interactions |