T cell epitopes in SARS-CoV-2 proteins are substantially conserved in the Omicron variant.

T cell epitopes in SARS-CoV-2 proteins are substantially conserved in the Omicron variant.
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DOI:
10.1038/s41423-022-00838-5
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发表时间:
2022-03
影响因子:
24.1
通讯作者:
Shin EC
Shin EC
中科院分区:
医学1区
文献类型:
--
作者:
Choi SJ;Kim DU;Noh JY;Kim S;Park SH;Jeong HW;Shin EC

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2021年11月,奥密克隆变种(B. 1.1. 529)出现并被世界卫生组织指定为关注变体(VOC)。最近,据报道,Omicron广泛逃避COVID-19疫苗接种或自然感染引起的中和抗体[1-3]。然而,Omicron是否逃避了COVID-19疫苗接种或自然感染引发的T细胞免疫仍有待阐明。为了解决这个问题,我们分析了从原始SARS-CoV-2毒株(武汉-胡-1)中鉴定的Omicron变体(hCoV-19/South Africa/CERI-KRISP-K 032284/2021)的T细胞表位的氨基酸序列。首先,我们检查了454个主要组织相容性复合体(MHC)I类限制性CD 8 + T细胞表位,这些表位先前通过活化诱导标记物(AIM)测定鉴定[4]。在Omicron变体中,来自刺突蛋白的88.4%(137/155)的表位和来自非刺突蛋白的98.3%(294/299)的表位是完全保守的(图1A),并且94.9%(431/454)的CD 8 + T细胞表位是完全保守的。我们对122个CD 8 + T细胞表位进行了类似的分析,这些表位先前通过使用肽-MHC I类复合物多聚体的系统分析鉴定[5]。在Omicron变异体中,来自刺突蛋白和非刺突蛋白的表位分别为88.9%(16/18)和98.1%(102/104),并且96.7%(118/122)的CD 8 + T细胞表位完全保守。我们通过对来自18项研究的852名COVID-19康复者的CD 8 + T细胞表位数据进行荟萃分析,确定了19个优势表位[6],所有19个CD 8 + T细胞表位在Omicron变体中完全保守。我们还检查了280个MHC II类限制性CD 4 + T细胞表位,这些表位先前通过AIM测定法鉴定[4]。在Omicron变异体中,来自刺突蛋白和非刺突蛋白的表位分别有80.4%(74/92)和94.7%(178/188)是完全保守的,并且90.0%(252/280)的CD 4 + T细胞表位是完全保守的。这些结果表明大多数T细胞表位在Omicron变体中相当保守。
In November 2021, the Omicron variant (B. 1.1. 529) emerged and was designated a variant of concern (VOC) by the World Health Organization. Recently, Omicron was reported to extensively escape neutralizing antibodies elicited by COVID-19 vaccination or natural infection [1-3]. However, whether Omicron evades the T cell immunity elicited by COVID-19 vaccination or natural infection remains to be elucidated. To address this issue, we analyzed the amino acid sequences of T cell epitopes identified from the original SARS-CoV-2 strain (Wuhan-Hu-1) in the Omicron variant (hCoV-19/South Africa/CERI-KRISP-K032284/2021). First, we examined 454 major histocompatibility complex (MHC) class I-restricted CD8+ T cell epitopes that were previously identified by activation-induced marker (AIM) assays [4]. In the Omicron variant, 88.4%(137/155) of epitopes from the spike protein and 98.3%(294/299) of epitopes from nonspike proteins were fully conserved (Fig. 1 A), and 94.9%(431/454) of CD8+ T cell epitopes were completely conserved. We performed a similar analysis with 122 CD8+ T cell epitopes that were previously identified by a systematic analysis using peptide-MHC class I complex multimers [5]. In the Omicron variant, 88.9%(16/18) and 98.1%(102/104) of epitopes from the spike and nonspike proteins, respectively, were fully conserved, and 96.7%(118/122) of CD8+ T cell epitopes were completely conserved. We identified 19 dominant epitopes by a meta-analysis of CD8+ T cell epitope data from 18 studies with 852 COVID-19 convalescents [6], and all 19 CD8+ T cell epitopes were completely conserved in the Omicron variant. We also examined 280 MHC class II-restricted CD4+ T cell epitopes that were previously identified by AIM assays [4]. In the Omicron variant, 80.4%(74/92) and 94.7%(178/188) of epitopes from the spike and nonspike proteins, respectively, were fully conserved, and 90.0%(252/280) of CD4+ T cell epitopes were completely conserved. These results indicate that the majority of T cell epitopes are considerably conserved in the Omicron variant.
DOI: 10.1126/sciimmunol.abf7550
发表时间: 2021-04-14
期刊: Science immunology
影响因子: 24.8
作者:
Saini SK;Hersby DS;Tamhane T;Povlsen HR;Amaya Hernandez SP;Nielsen M;Gang AO;Hadrup SR
通讯作者: Hadrup SR
DOI: 10.1038/s41577-021-00625-9
发表时间: 2021-11
期刊: Nature reviews. Immunology
影响因子: --
作者:
Noh JY;Jeong HW;Kim JH;Shin EC
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DOI: 10.1016/j.xcrm.2021.100312
发表时间: 2021-06-15
期刊: Cell reports. Medicine
影响因子: --
作者:
Quadeer AA;Ahmed SF;McKay MR
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DOI: 10.1038/s41586-021-03777-9
发表时间: 2021-07-08
期刊: NATURE
影响因子: 64.8
作者:
Planas, Delphine;Veyer, David;Schwartz, Olivier
通讯作者: Schwartz, Olivier
DOI: 10.1016/j.xcrm.2021.100204
发表时间: 2021-02-16
期刊: Cell reports. Medicine
影响因子: --
作者:
Tarke A;Sidney J;Kidd CK;Dan JM;Ramirez SI;Yu ED;Mateus J;da Silva Antunes R;Moore E;Rubiro P;Methot N;Phillips E;Mallal S;Frazier A;Rawlings SA;Greenbaum JA;Peters B;Smith DM;Crotty S;Weiskopf D;Grifoni A;Sette A
通讯作者: Sette A