Ancestral SARS-CoV-2-specific T cells cross-recognize the Omicron variant.
Ancestral SARS-CoV-2-specific T cells cross-recognize the Omicron variant.
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DOI：
10.1038/s41591-022-01700-x
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发表时间：
2022-03
期刊：
影响因子：
82.9
通讯作者：
Buggert M
中科院分区：
文献类型：
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作者：
Gao Y;Cai C;Grifoni A;Müller TR;Niessl J;Olofsson A;Humbert M;Hansson L;Österborg A;Bergman P;Chen P;Olsson A;Sandberg JK;Weiskopf D;Price DA;Ljunggren HG;Karlsson AC;Sette A;Aleman S;Buggert M
严重急性呼吸道综合征冠状病毒2型（SARS-CoV-2）Omicron（B.1.1.529）关注变体（VOC）的出现破坏了全球控制2019冠状病毒病（COVID-19）影响的努力。最近的数据表明，B.1.1.529可以很容易地感染具有自然获得或疫苗诱导免疫力的人，在某些情况下，通过中和祖先SARS-CoV-2的抗体的病毒逃逸来促进。然而，严重的疾病在这些个体中似乎相对罕见，突出了适应性免疫系统其他成分的潜在作用。我们在此报告，由先前感染或BNT 162 b2疫苗接种诱导的SARS-CoV-2刺突特异性CD 4+和CD 8 + T细胞提供了针对B.1.1.529的广泛免疫覆盖。在先前感染或接种BNT 162 b2的个体中，交叉识别B.1.1.529的SARS-CoV-2刺突特异性CD 4 + T细胞的中位相对频率分别为84%和91%，相应的SARS-CoV-2刺突特异性CD 8 + T细胞的中位相对频率分别为70%和92%。各组间的成对比较进一步揭示了SARS-CoV-2刺突反应性CD 4+和CD 8 + T细胞在功能和表型上对祖先菌株或B.1.1.529的反应相似。总的来说，我们的数据表明，已建立的SARS-CoV-2刺突特异性CD 4+和CD 8 + T细胞应答，特别是在BNT 162 b2疫苗接种后，对B.1.1.529基本保持完整。BNT 162 b2疫苗接种诱导的外周祖先SARS-CoV-2刺突特异性CD 4+和CD 8 + T细胞与Omicron变体的交叉反应水平高于先前SARS-CoV-2感染诱导的水平。
The emergence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron (B.1.1.529) variant of concern (VOC) has destabilized global efforts to control the impact of coronavirus disease 2019 (COVID-19). Recent data have suggested that B.1.1.529 can readily infect people with naturally acquired or vaccine-induced immunity, facilitated in some cases by viral escape from antibodies that neutralize ancestral SARS-CoV-2. However, severe disease appears to be relatively uncommon in such individuals, highlighting a potential role for other components of the adaptive immune system. We report here that SARS-CoV-2 spike-specific CD4+ and CD8+ T cells induced by prior infection or BNT162b2 vaccination provide extensive immune coverage against B.1.1.529. The median relative frequencies of SARS-CoV-2 spike-specific CD4+ T cells that cross-recognized B.1.1.529 in previously infected or BNT162b2-vaccinated individuals were 84% and 91%, respectively, and the corresponding median relative frequencies for SARS-CoV-2 spike-specific CD8+ T cells were 70% and 92%, respectively. Pairwise comparisons across groups further revealed that SARS-CoV-2 spike-reactive CD4+ and CD8+ T cells were functionally and phenotypically similar in response to the ancestral strain or B.1.1.529. Collectively, our data indicate that established SARS-CoV-2 spike-specific CD4+ and CD8+ T cell responses, especially after BNT162b2 vaccination, remain largely intact against B.1.1.529. Peripheral ancestral SARS-CoV-2 spike-specific CD4+ and CD8+ T cells induced by BNT162b2 vaccination cross-react to the Omicron variant at higher levels than those induced by prior SARS-CoV-2 infection.
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DOI：
10.1016/s0140-6736(22)00017-4
发表时间：
2022-01-29
期刊：
Lancet (London, England)
影响因子：
--
作者：
Wolter N;Jassat W;Walaza S;Welch R;Moultrie H;Groome M;Amoako DG;Everatt J;Bhiman JN;Scheepers C;Tebeila N;Chiwandire N;du Plessis M;Govender N;Ismail A;Glass A;Mlisana K;Stevens W;Treurnicht FK;Makatini Z;Hsiao NY;Parboosing R;Wadula J;Hussey H;Davies MA;Boulle A;von Gottberg A;Cohen C
通讯作者：
Cohen C
影响因子：
64.8
作者：
Oberhardt V;Luxenburger H;Kemming J;Schulien I;Ciminski K;Giese S;Csernalabics B;Lang-Meli J;Janowska I;Staniek J;Wild K;Basho K;Marinescu MS;Fuchs J;Topfstedt F;Janda A;Sogukpinar O;Hilger H;Stete K;Emmerich F;Bengsch B;Waller CF;Rieg S;Sagar;Boettler T;Zoldan K;Kochs G;Schwemmle M;Rizzi M;Thimme R;Neumann-Haefelin C;Hofmann M
通讯作者：
Hofmann M
影响因子：
11.1
作者：
Bergman P;Blennow O;Hansson L;Mielke S;Nowak P;Chen P;Söderdahl G;Österborg A;Smith CIE;Wullimann D;Vesterbacka J;Lindgren G;Blixt L;Friman G;Wahren-Borgström E;Nordlander A;Gomez AC;Akber M;Valentini D;Norlin AC;Thalme A;Bogdanovic G;Muschiol S;Nilsson P;Hober S;Loré K;Chen MS;Buggert M;Ljunggren HG;Ljungman P;Aleman S;COVAXID-collaborator group (shown separately)
通讯作者：
COVAXID-collaborator group (shown separately)
影响因子：
64.5
作者：
Moderbacher, Carolyn Rydyznski;Ramirez, Sydney, I;Crotty, Shane
通讯作者：
Crotty, Shane
影响因子：
24.8
作者：
通讯作者：
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