IRF9 缺陷患儿中，单克隆抗体介导的 SARS-CoV-2 中和作用。
Monoclonal antibody-mediated neutralization of SARS-CoV-2 in an IRF9-deficient child.
机构信息
Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM, Necker Hospital for Sick Children 75015 Paris, France.
Imagine Institute, University of Paris, Paris 75015, France.
出版信息
Proc Natl Acad Sci U S A. 2021 Nov 9;118(45). doi: 10.1073/pnas.2114390118.
We describe an unvaccinated child at risk for life-threatening COVID-19 due to an inherited deficiency of IRF9, which governs ISGF-3-dependent responses to type I and III interferons (IFN). She was admitted, with a high nasal SARS-CoV-2 load on day 1 of upper respiratory tract infection. She was viremic on day 2 and received casirivimab and imdevimab. Her clinical manifestations and viremia disappeared on days 3 and 4, respectively. Circulating SARS-CoV-2 virus induced the expression of IFN-stimulated genes in leukocytes on day 1, whereas the secretion of blood type I IFNs, which peaked on day 4, did not. Antibody-mediated SARS-CoV-2 neutralization is, therefore, sufficient to overcome a deficiency of antiviral IFNs.
我们描述了一名未接种疫苗的儿童，由于 IRF9 的遗传缺陷，她面临着危及生命的 COVID-19 风险，IRF9 调控着对 I 型和 III 型干扰素（IFN）的 ISGF-3 依赖性反应。该儿童因上呼吸道感染于入院第 1 天，鼻拭子 SARS-CoV-2 载量高。入院第 2 天，该儿童出现病毒血症，接受了 casirivimab 和 imdevimab 治疗。第 3 天和第 4 天，该儿童的临床表现和病毒血症分别消失。第 1 天，循环 SARS-CoV-2 病毒诱导白细胞中 IFN 刺激基因的表达，而第 4 天达到峰值的血液 I 型 IFNs 的分泌并未出现。因此，抗体介导的 SARS-CoV-2 中和足以克服抗病毒 IFN 的缺乏。
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