Department of Radiation Oncology, School of Medicine, University of California San Francisco, San Francisco, California, USA.
Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada.
Int J Med Sci. 2021 Oct 15;18(16):3788-3793. doi: 10.7150/ijms.61779. eCollection 2021.
As the world is racing to develop perpetual immunity to the SARS-CoV-2 virus. The emergence of new viral strains, together with vaccination and reinfections, are all contributing to a long-term immunity against the deadly virus that has taken over the world since its introduction to humans in late December 2019. The discovery that more than 95 percent of people who recovered from COVID-19 had long-lasting immunity and that asymptomatic people have a different immune response to SARS-CoV-2 than symptomatic people has shifted attention to how our immune system initiates such diverse responses. These findings have provided reason to believe that SARS-CoV-2 days are numbered. Hundreds of research papers have been published on the causes of long-lasting immune responses and variations in the numbers of different immune cell types in COVID 19 survivors, but the main reason of these differences has still not been adequately identified. In this article, we focus on the activation-induced cytidine deaminase (AID), which initiates molecular processes that allow our immune system to generate antibodies against SARS-CoV-2. To establish lasting immunity to SARS-CoV-2, we suggest that AID could be the key to unlocking it.
随着世界各国竞相开发针对 SARS-CoV-2 病毒的持久免疫力，新病毒株的出现，加上疫苗接种和再次感染，都在为长期免疫这种自 2019 年 12 月下旬在人类中出现以来肆虐全球的致命病毒做出贡献。研究发现，超过 95%的 COVID-19 康复者具有持久免疫力，无症状者对 SARS-CoV-2 的免疫反应与有症状者不同，这一发现将人们的注意力转向了我们的免疫系统如何引发这种多样化的反应。这些发现使人们有理由相信 SARS-CoV-2 的末日即将到来。已经有数百篇研究论文发表了关于持久免疫反应和 COVID-19 幸存者中不同免疫细胞类型数量变化的原因，但这些差异的主要原因仍未得到充分确定。在本文中，我们重点介绍了激活诱导胞苷脱氨酶（AID），它启动了分子过程，使我们的免疫系统能够产生针对 SARS-CoV-2 的抗体。为了建立针对 SARS-CoV-2 的持久免疫力，我们认为 AID 可能是解锁它的关键。
