作者
Roanne Keeton, Marius B Tincho, Amkele Ngomti, Richard Baguma, Ntombi Benede, Akiko Suzuki, Khadija Khan, Sandile Cele, Mallory Bernstein, Farina Karim, Sharon V Madzorera, Thandeka Moyo-Gwete, Mathilda Mennen, Sango Skelem, Marguerite Adriaanse, Daniel Mutithu, Olukayode Aremu, Cari Stek, Elsa Du Bruyn, Mieke A Van Der Mescht, Zelda de Beer, Talita R de Villiers, Annie Bodenstein, Gretha van den Berg, Adriano Mendes, Amy Strydom, Marietjie Venter, Jennifer Giandhari, Yeshnee Naidoo, Sureshnee Pillay, Houriiyah Tegally, Alba Grifoni, Daniela Weiskopf, Alessandro Sette, Robert J Wilkinson, Tulio de Oliveira, Linda-Gail Bekker, Glenda Gray, Veronica Ueckermann, Theresa Rossouw, Michael T Boswell, Jinal N Bhiman, Penny L Moore, Alex Sigal, Ntobeko AB Ntusi, Wendy A Burgers, Catherine Riou
发表日期
2022/3/17
期刊
Nature
卷号
603
期号
7901
页码范围
488-492
出版商
Nature Publishing Group UK
简介
The SARS-CoV-2 Omicron variant (B.1.1.529) has multiple spike protein mutations, that contribute to viral escape from antibody neutralization, , – and reduce vaccine protection from infection,. The extent to which other components of the adaptive response such as T cells may still target Omicron and contribute to protection from severe outcomes is unknown. Here we assessed the ability of T cells to react to Omicron spike protein in participants who were vaccinated with Ad26.CoV2.S or BNT162b2, or unvaccinated convalescent COVID-19 patients (n = 70). Between 70% and 80% of the CD4+ and CD8+ T cell response to spike was maintained across study groups. Moreover, the magnitude of Omicron cross-reactive T cells was similar for Beta (B.1.351) and Delta (B.1.617.2) variants, despite Omicron harbouring considerably more mutations. In patients who were hospitalized with Omicron infections (n = 19 …
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