啥叫ADE

，以及新冠病毒疫苗引起ADE的可能性，己有廣泛的討論

這篇文章應該有權威性，代表性。

https://www.nature.com/articles/s41564-020-00789-5

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Mechanisms of ADE

ADE has been documented to occur through two distinct mechanisms in viral infections: by enhanced antibody-mediated virus uptake into Fc gamma receptor IIa (FcγRIIa)-expressing phagocytic cells leading to increased viral infection and replication, or by excessive antibody Fc-mediated effector functions or immune complex formation causing enhanced inflammation and immunopathology (Fig. 1, Box 1). Both ADE pathways can occur when non-neutralizing antibodies or antibodies at sub-neutralizing levels bind to viral antigens without blocking or clearing infection. ADE can be measured in several ways, including in vitro assays (which are most common for the first mechanism involving FcγRIIa-mediated enhancement of infection in phagocytes), immunopathology or lung pathology. ADE via FcγRIIa-mediated endocytosis into phagocytic cells can be observed in vitro and has been extensively studied for macrophage-tropic viruses, including dengue virus in humans16 and FIPV in cats15. In this mechanism, non-neutralizing antibodies bind to the viral surface and traffic virions directly to macrophages, which then internalize the virions and become productively infected. Since many antibodies against different dengue serotypes are cross-reactive but non-neutralizing, secondary infections with heterologous strains can result in increased viral replication and more severe disease, leading to major safety risks as reported in a recent dengue vaccine trial13,14. In other vaccine studies, cats immunized against the FIPV S protein or passively infused with anti-FIPV antibodies had lower survival rates when challenged with FIPV compared to control groups17. Non-neutralizing antibodies, or antibodies at sub-neutralizing levels, enhanced entry into alveolar and peritoneal macrophages18, which were thought to disseminate infection and worsen disease outcome19.

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Conclusion

ADE has been observed in SARS, MERS and other human respiratory virus infections including RSV and measles, which suggests a real risk of ADE for SARS-CoV-2 vaccines and antibody-based interventions. However, clinical data has not yet fully established a role for ADE in human COVID-19 pathology. Steps to reduce the risks of ADE from immunotherapies include the induction or delivery of high doses of potent neutralizing antibodies, rather than lower concentrations of non-neutralizing antibodies that would be more likely to cause ADE.

Going forwards, it will be crucial to evaluate animal and clinical datasets for signs of ADE, and to balance ADE-related safety risks against intervention efficacy if clinical ADE is observed. Ongoing animal and human clinical studies will provide important insights into the mechanisms of ADE in COVID-19. Such evidence is sorely needed to ensure product safety in the large-scale medical interventions that are likely required to reduce the global burden of COVID-19.

 

要是嫌上麵的太囉嗦，這有個簡約通俗版的

https://www.cdc.gov/dengue/training/cme/ccm/page57857.html

 

 

所有跟帖： 

• 簡單的說 ADE 尚未觀查到，但ADE的風險現在沒法排除，尤其是對 delta, 以及 新的variant -三絲- ♂ (0 bytes) () 08/03/2021 postreply 18:34:14

• 如何降低風險，是打第booster嗎？ -三絲- ♂ (0 bytes) () 08/03/2021 postreply 18:35:22

• 這是個 risk vs benefit 大小的問題。 -三絲- ♂ (0 bytes) () 08/03/2021 postreply 18:37:39

• 多謝夫子兄分享. 多多保重！ -kingfish2010- ♂ (0 bytes) () 08/04/2021 postreply 02:06:58