Pseudotyped Bat Coronavirus RaTG13 is efficiently neutralised by convalescent sera from SARS-CoV-2 infected patients.
Pseudotyped Bat Coronavirus RaTG13 is efficiently neutralised by convalescent sera from SARS-CoV-2 infected patients.
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伪型蝙蝠冠状病毒Ratg13被SARS-COV-2感染患者的康复血清有效中和。
DOI：
10.1038/s42003-022-03325-9
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发表时间：
2022-05-03
影响因子：
5.9
通讯作者：
中科院分区：
文献类型：
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作者：
RaTG13 is a close relative of SARS-CoV-2, the virus responsible for the COVID-19 pandemic, sharing 96% sequence similarity at the genome-wide level. The spike receptor binding domain (RBD) of RaTG13 contains a number of amino acid substitutions when compared to SARS-CoV-2, likely impacting affinity for the ACE2 receptor. Antigenic differences between the viruses are less well understood, especially whether RaTG13 spike can be efficiently neutralised by antibodies generated from infection with, or vaccination against, SARS-CoV-2. Using RaTG13 and SARS-CoV-2 pseudotypes we compared neutralisation using convalescent sera from previously infected patients or vaccinated healthcare workers. Surprisingly, our results revealed that RaTG13 was more efficiently neutralised than SARS-CoV-2. In addition, neutralisation assays using spike mutants harbouring single and combinatorial amino acid substitutions within the RBD demonstrated that both spike proteins can tolerate multiple changes without dramatically reducing neutralisation. Moreover, introducing the 484 K mutation into RaTG13 resulted in increased neutralisation, in contrast to the same mutation in SARS-CoV-2 (E484K). This is despite E484K having a well-documented role in immune evasion in variants of concern (VOC) such as B.1.351 (Beta). These results indicate that the future spill-over of RaTG13 and/or related sarbecoviruses could be mitigated using current SARS-CoV-2-based vaccination strategies. Bat Coronavirus RaTG13, a sarbecovirus related to SARS-CoV-2, is more potently neutralized by antibodies from convalescent SARS-CoV-2-infected patients as well as vaccinated healthcare workers despite the spike proteins having high diversity within their receptor binding domains (RBD).
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影响因子：
64.8
作者：
Saunders KO;Lee E;Parks R;Martinez DR;Li D;Chen H;Edwards RJ;Gobeil S;Barr M;Mansouri K;Alam SM;Sutherland LL;Cai F;Sanzone AM;Berry M;Manne K;Bock KW;Minai M;Nagata BM;Kapingidza AB;Azoitei M;Tse LV;Scobey TD;Spreng RL;Rountree RW;DeMarco CT;Denny TN;Woods CW;Petzold EW;Tang J;Oguin TH 3rd;Sempowski GD;Gagne M;Douek DC;Tomai MA;Fox CB;Seder R;Wiehe K;Weissman D;Pardi N;Golding H;Khurana S;Acharya P;Andersen H;Lewis MG;Moore IN;Montefiori DC;Baric RS;Haynes BF
通讯作者：
Haynes BF
影响因子：
64.5
作者：
Thomson EC;Rosen LE;Shepherd JG;Spreafico R;da Silva Filipe A;Wojcechowskyj JA;Davis C;Piccoli L;Pascall DJ;Dillen J;Lytras S;Czudnochowski N;Shah R;Meury M;Jesudason N;De Marco A;Li K;Bassi J;O'Toole A;Pinto D;Colquhoun RM;Culap K;Jackson B;Zatta F;Rambaut A;Jaconi S;Sreenu VB;Nix J;Zhang I;Jarrett RF;Glass WG;Beltramello M;Nomikou K;Pizzuto M;Tong L;Cameroni E;Croll TI;Johnson N;Di Iulio J;Wickenhagen A;Ceschi A;Harbison AM;Mair D;Ferrari P;Smollett K;Sallusto F;Carmichael S;Garzoni C;Nichols J;Galli M;Hughes J;Riva A;Ho A;Schiuma M;Semple MG;Openshaw PJM;Fadda E;Baillie JK;Chodera JD;ISARIC4C Investigators;COVID-19 Genomics UK (COG-UK) Consortium;Rihn SJ;Lycett SJ;Virgin HW;Telenti A;Corti D;Robertson DL;Snell G
通讯作者：
Snell G
DOI：
10.1126/science.abf9302
发表时间：
2021-02-19
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Starr TN;Greaney AJ;Addetia A;Hannon WW;Choudhary MC;Dingens AS;Li JZ;Bloom JD
通讯作者：
Bloom JD
影响因子：
7.3
作者：
Cantoni D;Mayora-Neto M;Nadesalingam A;Wells DA;Carnell GW;Ohlendorf L;Ferrari M;Palmer P;Chan ACY;Smith P;Bentley EM;Einhauser S;Wagner R;Page M;Raddi G;Baxendale H;Castillo-Olivares J;Heeney J;Temperton N
通讯作者：
Temperton N
影响因子：
7.3
作者：
Castillo-Olivares J;Wells DA;Ferrari M;Chan ACY;Smith P;Nadesalingam A;Paloniemi M;Carnell GW;Ohlendorf L;Cantoni D;Mayora-Neto M;Palmer P;Tonks P;Temperton NJ;Peterhoff D;Neckermann P;Wagner R;Doffinger R;Kempster S;Otter AD;Semper A;Brooks T;Albecka A;James LC;Page M;Schwaeble W;Baxendale H;Heeney JL
通讯作者：
Heeney JL