Genetically diverse mouse models of SARS-CoV-2 infection reproduce clinical variation in type I interferon and cytokine responses in COVID-19.
Genetically diverse mouse models of SARS-CoV-2 infection reproduce clinical variation in type I interferon and cytokine responses in COVID-19.
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DOI：
10.1038/s41467-023-40076-5
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发表时间：
2023-07-25
影响因子：
16.6
通讯作者：
Best, Sonja M.
中科院分区：
文献类型：
--
作者：
Robertson, Shelly J.;Bedard, Olivia;McNally, Kristin L.;Shaia, Carl;Clancy, Chad S.;Lewis, Matthew;Broeckel, Rebecca M.;Chiramel, Abhilash I.;Shannon, Jeffrey G.;Sturdevant, Gail L.;Rosenke, Rebecca;Anzick, Sarah L.;Forte, Elvira;Preuss, Christoph;Baker, Candice N.;Harder, Jeffrey M.;Brunton, Catherine;Munger, Steven;Bruno, Daniel P.;Lack, Justin B.;Leung, Jacqueline M.;Shamsaddini, Amirhossein;Gardina, Paul;Sturdevant, Daniel E.;Sun, Jian;Martens, Craig;Holland, Steven M.;Rosenthal, Nadia A.;Best, Sonja M.
Inflammation in response to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection drives severity of coronavirus disease 2019 (COVID-19) and is influenced by host genetics. To understand mechanisms of inflammation, animal models that reflect genetic diversity and clinical outcomes observed in humans are needed. We report a mouse panel comprising the genetically diverse Collaborative Cross (CC) founder strains crossed to human ACE2 transgenic mice (K18-hACE2) that confers susceptibility to SARS-CoV-2. Infection of CC x K18-hACE2 resulted in a spectrum of survival, viral replication kinetics, and immune profiles. Importantly, in contrast to the K18-hACE2 model, early type I interferon (IFN-I) and regulated proinflammatory responses were required for control of SARS-CoV-2 replication in PWK x K18-hACE2 mice that were highly resistant to disease. Thus, virus dynamics and inflammation observed in COVID-19 can be modeled in diverse mouse strains that provide a genetically tractable platform for understanding anti-coronavirus immunity. Dynamics of type I interferon (IFN) following infection with SARS-CoV-2 are critical in determining disease severity in humans but have been difficult to model in mice. Here, infection of genetically diverse mice reveals how delayed or immediate IFN signaling coordinates antiviral immunity.
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影响因子：
64.8
作者：
Muñoz-Fontela C;Dowling WE;Funnell SGP;Gsell PS;Riveros-Balta AX;Albrecht RA;Andersen H;Baric RS;Carroll MW;Cavaleri M;Qin C;Crozier I;Dallmeier K;de Waal L;de Wit E;Delang L;Dohm E;Duprex WP;Falzarano D;Finch CL;Frieman MB;Graham BS;Gralinski LE;Guilfoyle K;Haagmans BL;Hamilton GA;Hartman AL;Herfst S;Kaptein SJF;Klimstra WB;Knezevic I;Krause PR;Kuhn JH;Le Grand R;Lewis MG;Liu WC;Maisonnasse P;McElroy AK;Munster V;Oreshkova N;Rasmussen AL;Rocha-Pereira J;Rockx B;Rodríguez E;Rogers TF;Salguero FJ;Schotsaert M;Stittelaar KJ;Thibaut HJ;Tseng CT;Vergara-Alert J;Beer M;Brasel T;Chan JFW;García-Sastre A;Neyts J;Perlman S;Reed DS;Richt JA;Roy CJ;Segalés J;Vasan SS;Henao-Restrepo AM;Barouch DH
通讯作者：
Barouch DH
影响因子：
7.6
作者：
Gan ES;Syenina A;Linster M;Ng B;Zhang SL;Watanabe S;Rajarethinam R;Tan HC;Smith GJ;Ooi EE
通讯作者：
Ooi EE
危及生命的Covid-19患者中针对I型IFN的自身抗体。
DOI：
10.1126/science.abd4585
发表时间：
2020-10-23
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Bastard P;Rosen LB;Zhang Q;Michailidis E;Hoffmann HH;Zhang Y;Dorgham K;Philippot Q;Rosain J;Béziat V;Manry J;Shaw E;Haljasmägi L;Peterson P;Lorenzo L;Bizien L;Trouillet-Assant S;Dobbs K;de Jesus AA;Belot A;Kallaste A;Catherinot E;Tandjaoui-Lambiotte Y;Le Pen J;Kerner G;Bigio B;Seeleuthner Y;Yang R;Bolze A;Spaan AN;Delmonte OM;Abers MS;Aiuti A;Casari G;Lampasona V;Piemonti L;Ciceri F;Bilguvar K;Lifton RP;Vasse M;Smadja DM;Migaud M;Hadjadj J;Terrier B;Duffy D;Quintana-Murci L;van de Beek D;Roussel L;Vinh DC;Tangye SG;Haerynck F;Dalmau D;Martinez-Picado J;Brodin P;Nussenzweig MC;Boisson-Dupuis S;Rodríguez-Gallego C;Vogt G;Mogensen TH;Oler AJ;Gu J;Burbelo PD;Cohen JI;Biondi A;Bettini LR;D'Angio M;Bonfanti P;Rossignol P;Mayaux J;Rieux-Laucat F;Husebye ES;Fusco F;Ursini MV;Imberti L;Sottini A;Paghera S;Quiros-Roldan E;Rossi C;Castagnoli R;Montagna D;Licari A;Marseglia GL;Duval X;Ghosn J;HGID Lab;NIAID-USUHS Immune Response to COVID Group;COVID Clinicians;COVID-STORM Clinicians;Imagine COVID Group;French COVID Cohort Study Group;Milieu Intérieur Consortium;CoV-Contact Cohort;Amsterdam UMC Covid-19 Biobank;COVID Human Genetic Effort;Tsang JS;Goldbach-Mansky R;Kisand K;Lionakis MS;Puel A;Zhang SY;Holland SM;Gorochov G;Jouanguy E;Rice CM;Cobat A;Notarangelo LD;Abel L;Su HC;Casanova JL
通讯作者：
Casanova JL
影响因子：
64.8
作者：
Delorey TM;Ziegler CGK;Heimberg G;Normand R;Yang Y;Segerstolpe Å;Abbondanza D;Fleming SJ;Subramanian A;Montoro DT;Jagadeesh KA;Dey KK;Sen P;Slyper M;Pita-Juárez YH;Phillips D;Biermann J;Bloom-Ackermann Z;Barkas N;Ganna A;Gomez J;Melms JC;Katsyv I;Normandin E;Naderi P;Popov YV;Raju SS;Niezen S;Tsai LT;Siddle KJ;Sud M;Tran VM;Vellarikkal SK;Wang Y;Amir-Zilberstein L;Atri DS;Beechem J;Brook OR;Chen J;Divakar P;Dorceus P;Engreitz JM;Essene A;Fitzgerald DM;Fropf R;Gazal S;Gould J;Grzyb J;Harvey T;Hecht J;Hether T;Jané-Valbuena J;Leney-Greene M;Ma H;McCabe C;McLoughlin DE;Miller EM;Muus C;Niemi M;Padera R;Pan L;Pant D;Pe'er C;Pfiffner-Borges J;Pinto CJ;Plaisted J;Reeves J;Ross M;Rudy M;Rueckert EH;Siciliano M;Sturm A;Todres E;Waghray A;Warren S;Zhang S;Zollinger DR;Cosimi L;Gupta RM;Hacohen N;Hibshoosh H;Hide W;Price AL;Rajagopal J;Tata PR;Riedel S;Szabo G;Tickle TL;Ellinor PT;Hung D;Sabeti PC;Novak R;Rogers R;Ingber DE;Jiang ZG;Juric D;Babadi M;Farhi SL;Izar B;Stone JR;Vlachos IS;Solomon IH;Ashenberg O;Porter CBM;Li B;Shalek AK;Villani AC;Rozenblatt-Rosen O;Regev A
通讯作者：
Regev A
影响因子：
16
作者：
Martin-Sancho L;Lewinski MK;Pache L;Stoneham CA;Yin X;Becker ME;Pratt D;Churas C;Rosenthal SB;Liu S;Weston S;De Jesus PD;O'Neill AM;Gounder AP;Nguyen C;Pu Y;Curry HM;Oom AL;Miorin L;Rodriguez-Frandsen A;Zheng F;Wu C;Xiong Y;Urbanowski M;Shaw ML;Chang MW;Benner C;Hope TJ;Frieman MB;García-Sastre A;Ideker T;Hultquist JF;Guatelli J;Chanda SK
通讯作者：
Chanda SK