Antibody-dependent enhancement (ADE) is a mechanism by which the pathogenesis of certain viral infections is enhanced in the presence of sub-neutralizing or cross-reactive non-neutralizing antiviral antibodies. In vitro modelling of ADE has attributed enhanced pathogenesis to Fcγ receptor (FcγR)-mediated viral entry, rather than canonical viral receptor-mediated entry. However, the putative FcγR-dependent mechanisms of ADE overlap with the role of these receptors in mediating antiviral protection in various viral infections, necessitating a detailed understanding of how this diverse family of receptors functions in protection and pathogenesis. Here, we discuss the diversity of immune responses mediated upon FcγR engagement and review the available experimental evidence supporting the role of FcγRs in antiviral protection and pathogenesis through ADE. We explore FcγR engagement in the context of a range of different viral infections, including dengue virus and SARS-CoV, and consider ADE in the context of the ongoing SARS-CoV-2 pandemic.

抗体依赖性增强（ADE）是一种机制，在亚中和或交叉反应的非中和抗病毒抗体存在下，某些病毒感染的发病机理得以增强。ADE的体外建模将发病机制的增强归因于Fcγ受体（FcγR）介导的病毒进入，而不是规范的病毒受体介导的进入。但是，假定的FcγR依赖性ADE机制与这些受体在各种病毒感染中介导抗病毒保护的作用重叠，因此有必要详细了解这种受体家族在保护和发病机理中的功能。这里，我们讨论了由FcγR参与介导的免疫反应的多样性，并回顾了可利用的实验证据支持FcγR在ADE中的抗病毒保护和发病机理中的作用。我们在一系列不同的病毒感染（包括登革热病毒和SARS-CoV）的背景下探索FcγR参与，并在正在进行的SARS-CoV-2大流行的背景下考虑ADE。