Sawant Jyoti, Patil Ajit, Kurle Swarali
HIV Drug Resistance Laboratory, ICMR-National AIDS Research Institute, Pune 411026, India.
Vaccines (Basel). 2023 Jul 14;11(7):1240. doi: 10.3390/vaccines11071240.
Antibody Dependent Enhancement (ADE) of an infection has been of interest in the investigation of many viruses. It is associated with the severity of the infection. ADE is mediated by non-neutralizing antibodies, antibodies at sub-neutralizing concentrations, or cross-reactive non-neutralizing antibodies. Treatments like plasma therapy, B cell immunizations, and antibody therapies may trigger ADE. It is seen as an impediment to vaccine development as well. In viruses including the Dengue virus (DENV), severe acute respiratory syndrome (SARS) virus, Middle East respiratory syndrome (MERS) virus, human immunodeficiency virus (HIV), Ebola virus, Zika virus, and influenza virus, the likely mechanisms of ADE are postulated and described. ADE improves the likelihood of productively infecting cells that are expressing the complement receptor or the Fc receptor (FcR) rather than the viral receptors. ADE occurs when the FcR, particularly the Fc gamma receptor, and/or complement system, particularly Complement 1q (C1q), allow the entry of the virus-antibody complex into the cell. Moreover, ADE alters the innate immune pathways to escape from lysis, promoting viral replication inside the cell that produces viral particles. This review discusses the involvement of FcR and the downstream immunomodulatory pathways in ADE, the complement system, and innate antiviral signaling pathways modification in ADE and its impact on facilitating viral replication. Additionally, we have outlined the modes of ADE in the cases of different viruses reported until now.
感染的抗体依赖增强（ADE）在许多病毒的研究中备受关注。它与感染的严重程度相关。ADE由非中和抗体、亚中和浓度的抗体或交叉反应性非中和抗体介导。血浆疗法、B细胞免疫和抗体疗法等治疗方法可能引发ADE。它也被视为疫苗开发的一个障碍。在包括登革热病毒（DENV）、严重急性呼吸综合征（SARS）病毒、中东呼吸综合征（MERS）病毒、人类免疫缺陷病毒（HIV）、埃博拉病毒、寨卡病毒和流感病毒在内的病毒中，ADE的可能机制已被提出并描述。ADE提高了有效感染表达补体受体或Fc受体（FcR）而非病毒受体的细胞的可能性。当FcR，特别是Fcγ受体，和/或补体系统，特别是补体1q（C1q）允许病毒 - 抗体复合物进入细胞时，ADE就会发生。此外，ADE改变固有免疫途径以逃避裂解，促进病毒在产生病毒颗粒的细胞内复制。这篇综述讨论了FcR和下游免疫调节途径在ADE中的作用、补体系统以及ADE中固有抗病毒信号通路的改变及其对促进病毒复制的影响。此外，我们概述了迄今为止报道的不同病毒病例中的ADE模式。
