Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA.
Department of Pathology and Immunology, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA.
Med. 2022 May 13;3(5):309-324.e6. doi: 10.1016/j.medj.2022.03.009. Epub 2022 Apr 15.
Since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in 2019, viral variants with greater transmissibility or immune-evasion properties have arisen, which could jeopardize recently deployed vaccine- and antibody-based countermeasures.
Here, we evaluated in mice and hamsters the efficacy of a pre-clinical version of the Moderna mRNA vaccine (mRNA-1273) and the Johnson & Johnson recombinant adenoviral-vectored vaccine (Ad26.COV2.S) against the B.1.621 (Mu) variant of SARS-CoV-2, which contains spike mutations T95I, Y144S, Y145N, R346K, E484K, N501Y, D614G, P681H, and D950N.
Immunization of 129S2 and K18-human ACE2 transgenic mice with the mRNA-1273 vaccine protected against weight loss, lung infection, and lung pathology after challenge with the B.1.621 or WA1/2020 N501Y/D614G SARS-CoV-2 strain. Similarly, immunization of 129S2 mice and Syrian hamsters with a high dose of Ad26.COV2.S reduced lung infection after B.1.621 virus challenge.
Thus, immunity induced by the mRNA-1273 or Ad26.COV2.S vaccine can protect against the B.1.621 variant of SARS-CoV-2 in multiple animal models.
This study was supported by the NIH (R01 AI157155 and U01 AI151810), NIAID Centers of Excellence for Influenza Research and Response [CEIRR] contracts 75N93021C00014 and 75N93021C00016, and the Collaborative Influenza Vaccine Innovation Centers [CIVIC] contract 75N93019C00051. It was also supported, in part, by the National Institutes of Allergy and Infectious Diseases Center for Research on Influenza Pathogenesis (HHSN272201400008C) and the Japan Program for Infectious Diseases Research and Infrastructure (JP21wm0125002) from the Japan Agency for Medical Research and Development (AMED).
自 2019 年严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2)出现以来,出现了具有更高传染性或免疫逃逸特性的病毒变体,这可能危及最近部署的疫苗和抗体为基础的对策。
在这里,我们在小鼠和仓鼠中评估了现代 mRNA 疫苗(mRNA-1273)和强生公司的重组腺病毒载体疫苗(Ad26.COV2.S)对 B.1.621 (Mu)变体的功效,SARS-CoV-2,其中包含 Spike 突变 T95I、Y144S、Y145N、R346K、E484K、N501Y、D614G、P681H 和 D950N。
用 mRNA-1273 疫苗免疫 129S2 和 K18 人血管紧张素转换酶 2 转基因小鼠,可预防 B.1.621 或 WA1/2020 N501Y/D614G SARS-CoV-2 株感染后体重减轻、肺部感染和肺部病理学改变。同样,用高剂量 Ad26.COV2.S 免疫 129S2 小鼠和叙利亚仓鼠可减少 B.1.621 病毒感染后的肺部感染。
因此,mRNA-1273 或 Ad26.COV2.S 疫苗诱导的免疫可以保护多种动物模型免受 SARS-CoV-2 的 B.1.621 变体的侵害。
本研究由 NIH(R01 AI157155 和 U01 AI151810)、NIAID 传染病卓越研究中心[CEIRR]合同 75N93021C00014 和 75N93021C00016 以及合作流感疫苗创新中心[CIVIC]合同 75N93019C00051 资助。它还得到了美国国立过敏和传染病研究所流感发病机制研究中心(HHSN272201400008C)和日本传染病研究与基础设施计划(JP21wm0125002)的部分支持,该计划由日本医疗研究与发展署(AMED)资助。