31 research outputs found
Shear Banding of Soft Glassy Materials in Large Amplitude Oscillatory Shear
- Publication venue
- American Physical Society
- Publication date
- 13/10/2016
- Field of study
We study shear banding in soft glassy materials subject to a large amplitude oscillatory shear flow (LAOS). By numerical simulations of the widely used soft glassy rheology model, supplemented by more general physical arguments, we demonstrate strong banding over an extensive range of amplitudes and frequencies of the imposed shear rate γ˙(t)=γ˙0cos(ωt), even in materials that do not permit banding as their steady state response to a steadily imposed shear flow γ˙=γ˙0=const. Highly counterintuitively, banding persists in LAOS even in the limit of zero frequency ω→0, where one might a priori have expected a homogeneous flow response in a material that does not display banding under conditions of steadily imposed shear. We explain this finding in terms of an alternating competition within each cycle between glassy aging and flow rejuvenation. Our predictions have far-reaching implications for the flow behavior of aging yield stress fluids, suggesting a generic expectation of shear banding in flows of even arbitrarily slow time variation
Shear Banding of Soft Glassy Materials in Large Amplitude Oscillatory Shear
- Publication venue
- 'American Physical Society (APS)'
- Publication date
- Field of study
Influence of shear on globule formation in dilute solutions of flexible polymers
- Publication venue
- 'AIP Publishing'
- Publication date
- Field of study
Needle(s) in the Haystack – Synchronous Multifocal Tumor Induced Osteomalacia
- Author
- Annamalai Anand K.
- Chelian Mathirajan
- Clifton-Bligh Roderick
- Gill Anthony J.
- Gopalakrishnan Chandrasekhar
- Gurnell Mark
- Kane Shubhada
- Kulkarni Suyash
- Mahuvakar Ankit D.
- Pai Prathamesh S.
- Purandare Nilendu
- Puri Vipla
- Rangarajan Venkatesh
- Sampathkumar Krishnaswamy
- Shanthi Radhakrishnan
- Shetty Nitin S.
- Srinivasan K. G.
- Subramaniam Aram
- Suriyakumar Govindarajulu
- Publication venue
- The Journal of Clinical Endocrinology & Metabolism
- Publication date
- 21/12/2015
- Field of study
This is the author accepted manuscript. The final version is available from Endocrine Society via http://dx.doi.org/10.1210/jc.2015-3854MG is supported by the NIHR Cambridge Biomedical Research Centre
Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.
- Author
- Aamir A
- Abbas J
- Abbas N
- Abbott TEF
- Abdalla M
- Abdikadir H
- Abuhussein N
- Acquaah F
- Adamson R
- Adeleye O
- Adeogun A
- Adlan A
- Aftab R
- Afzal Z
- Agarwal M
- Aglan H
- Agnew CJF
- Agrawal R
- Ahern D
- Ahluwalia J
- Ahluwalia V
- Ahmad A
- Ahmad K
- Ahmed H
- Ahmed I
- Ahmed L
- Ahmed N
- Ahmed P
- Ainger E
- Ainsworth P
- Aishwarya G
- Ajibola-Taylor O
- Akhbari M
- Akhtar A
- Akhtar R
- Akpenyi O
- Al-Ausi M
- Al-Huneidi R
- Al-Khudairi R
- Al-Masri S
- Al-Mousawi A
- Al-Saadi N
- Alagappan A
- Alberts J
- Alfa-Wali M
- Ali A
- Ali B
- Ali I
- Ali M
- Ali Q
- Ali S
- Alturki N
- Alwandi A
- Amani L
- Amarnath T
- Amer M
- Amin H
- Amin MN
- Amoah R
- Amoah-Arko A
- Anandarajah C
- Ananthavarathan P
- Andah EJE
- Andrew K
- Andrews H
- Ang A
- Ang HL
- Ang JJ
- Ani C
- Anilkumar A
- Anto N
- Anwar S
- Apperley H
- Appleton S
- Aquilina T
- Archer M
- Arif T
- Arneill M
- Arnell S
- Arnold TJ
- Arshad A
- Arthur J
- Arulkumaran N
- Arya J
- Asad M
- Asemota N
- Ashaye T
- Ashdown T
- Ashour R
- Ashraf MR
- Ashwood J
- Asif U
- Atkin G
- Atkins B
- Attalla M
- Aubrey-Jones D
- Auckburally S
- Auld F
- Auluck I
- Azam S
- Aziz R
- Azizi A
- Azmi F
- Babatunde F
- Babu VS
- Bachi A
- Bagga R
- Bains H
- Bajwa DS
- Baker A
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- Balai E
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- Bamford M
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- Bannard-Smith J
- Barai I
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- Barnfield J
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- Barraclough J
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- Siddiqui I
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- STARSurg Collaborative Writing Committee, Data analysis, Steering committee, Advisory group, Regional leads, Collaborators and validators
- STARSurg Collaborative Writing Committee, Data analysis, Steering committee, Advisory group, Regional leads, Collaborators and validators, Nepogodiev, D
- Stechman M
- Stewart D
- Stewart E
- Stewart H
- Stewart R
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- Stoddart MT
- Stokes E
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- Strang S
- Stringer H
- Stringfellow TD
- Stubbing-Moore A
- Sturrock S
- Subar D
- Subratty SM
- Sukirthan N
- Sukumar S
- Sulaiman SK
- Sultan S
- Sun L
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- Suresh R
- Suresh S
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- Yahaya AA
- Yalamarthi S
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- Yarham E
- Yasin IH
- Yasin T
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- Yeung J
- Yin ZD
- Yip J
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- Yousaf A
- Youssef H
- Yu T
- Yule A
- Zaat S
- Zanichelli D
- Zaver V
- Zeng R
- Zhang Y
- Zheleniakova T
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- Zornoza A
- Zubikarai G
- Zulkifli A
- Zuzarte L
- Publication venue
- 'Wiley'
- Publication date
- 18/05/2018
- Field of study
Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14·2 per cent (646 of 4544) and the 30-day mortality rate was 1·8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7·61, 95 per cent c.i. 4·49 to 12·90; P < 0·001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0·65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability
AI is a viable alternative to high throughput screening: a 318-target study
- Author
- Abaffy Tatjana
- Abraham Elena Theres
- Abrahão Jônatas Santos
- Abramyan Tigran M.
- Agianian Bogos
- Agogo-Mawuli Percy
- Agoulnik Alexander I.
- Agrawal Rajendra K.
- Aguilera Elena
- Ahmed Mostafa
- Akk Gustav
- Akopian Tatos
- Al-Yozbaki Minnatallah
- Aldhamen Yasser Ali
- Alkan Cigdem
- Alramadhani Dina
- Alteen Matthew G.
- Alvarez Guzmán
- Ammendola Serena
- Anastasio Noelle C.
- Anderson Brandon M.
- Anderson Deborah H.
- Andricopulo Adriano D.
- Angell Richard M.
- Anthis Nicholas J.
- Antonelli Lorenzo
- Apfel Athena Marie
- Arias Juan Antonio Sanchez
- Arozarena Imanol
- Arrigoni Cristina
- Artía Zoraima
- Ashkar Shireen R.
- Ashton Mark R.
- Austin Richard C.
- Ayachi Aicha Gharbi
- Azeem Syeda Maryam
- Bailey-Elkin Ben A.
- Balakrishnan Bijina
- Balaña-Fouce Rafael
- Ballatore Carlo
- Banerjee Sourav
- Banerji Versha
- Banjo Toshihiro
- Barghash Marim M.
- Batey Robert A.
- Battistoni Andrea
- Baumann Ulrich
- Bdira Fredj Ben
- Bedi Mel
- Ben-Johny Manu
- Bergman Bastiaan
- Bernard Denzil
- Berti Andrew
- Bharambe Nikhil
- Bishop Ozlem Tastan
- Blanchet Xavier
- Blelloch Robert
- Blumenthal Robert M.
- Bognár Gabriella
- Bogomolovas Julijus
- Bon Carlotta
- Boorman Jacob
- Borowska Anna
- Borriello Francesco
- Bowman Gregory R.
- Bradley Robert K.
- Bradshaw William J.
- Brady-Kalnay Susann M.
- Breton Hairol E.
- Bruning John B.
- Bruning John Burt
- Bryant-Friedrich Amanda
- Buckner Frederick S.
- Buroni Silvia
- Butler Brittany
- Byrne Lee J.
- Byun Soo Young
- Caflisch Amedeo
- Cakir Isin
- Caliandro Ileana
- Caljon Guy
- Cann Andrew B.
- Caporali Andrea
- Capuzzi Stephen J.
- Caroleo Maria Cristina
- Cathcart Ann M.
- Celano Stephanie L.
- Cerna Mark Vincent C. dela
- Chadni Somaia Haque
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- Chan Nei-Li
- Chapman Carly J.
- Chaton Catherine T.
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- Chaudhuri Dipayan
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- Chaytow Helena
- Chen Daniel
- Chen Lifeng
- Chen Yicheng
- Chern Ting-Rong
- Chini Andrea
- Chou Tristan
- Chou Tsui-Fen
- Christensen Emily M.
- Christodoulides Myron
- Chu Shaoyou
- Chua Benjamin Soon Kai
- Chuah Janelle
- Chung Zara
- Chuong Patrick
- Ciccia Alberto
- Cildir Gökhan
- Cione Erika
- Clayton W. Brent
- Coles John G.
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- Conn Graeme L.
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- Contreras Stephanie
- Cools Julie
- Coombe Deirdre R.
- Corson Timothy W.
- Cortopassi Gino
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- Cowen Leah E.
- Cox Bryan D.
- Cuddihy Andrew R.
- Cullinane Ryan T.
- Cunningham Kathryn A.
- Dahal Gopal
- Dallman Sydney
- Dame Remus T.
- Davtyan Aram
- De Keulenaer Gilles
- De Luise Monica
- de Oliveira Aldo Sena
- de Oliveira Saulo
- de Sousa Alessandra Mara
- de Souza Guilherme Eduardo
- Debonsi Hosana Maria
- Degterev Alexei
- DeHaan Nicholas
- Del Rio Flores Antonio
- Dempsey Garrett
- Desai Umesh R.
- Diallo Bakary N’tji
- Dickhout Jeffrey
- Dickinson Bryan C.
- Dieck Chelsea L.
- Dirksen Dorian
- do Monte-Neto Rubens Lima
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- D’Antuono Anna
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- Kushnir Alexander
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- Lai Kent
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- Lenci Elena
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- Lisabeth Erika Mathes
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- Matovic Nick
- Mattevi Andrea
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- Mayer Gaétan
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- McDowell Mary Ann
- McManus Kirk James
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- Mehlman Tamar
- Mellado Mario
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- Mushtaq Aisha
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- Myhr Courtney
- Mysinger Michael
- Mysore Venkatesh
- Nagai Maira Harume
- Nagamori Kiyo
- Namasivayam Vigneshwaran
- Nasburg Joshua Alexander
- Ng Ho Leung
- Ng James
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- Nguyen Kong
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- null null
- Ogunwa Tomisin Happy
- Ojha Anil K.
- Ojo Kayode K.
- Olson Steven H.
- Ortiz Diana
- Oyarzabal Julen
- O’Brien Terrence E.
- O’Connell Patrick
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- Phadke Sameer
- Pham Kien
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- Poirier Steve
- Popowicz Grzegorz Maria
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- PrasadPrasad Srimukh Veccham Krishna
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- Prikler Gergely
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- Puchades-Carrasco Leonor
- Pusztai Lajos
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- Rabal Obdulia
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- Rayman Joseph B.
- Reglero Clara
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- Reis Joana
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- Riches David W. H.
- Rizzi Menico
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- Rodriguez G. Marcela
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- Skorodinsky Maxim
- Slotboom Dirk J.
- Smith David M.
- Smith Kristiana S.
- Smrcka Alan V.
- So Jonathan
- Sobrado Pablo
- Soellner Matthew B.
- Solano Roberto
- Sorenson Jon M.
- Stafford Kate
- Stahl Andreas
- Statsyuk Alexander V.
- Stec Natalia
- Stecula Adrian
- Stetefeld Joerg
- Strauss Erick
- Stuchbury Grant David
- Su Leila
- Su Tong
- Su Zhengchen
- Sugamori Kim S.
- Sun Ying
- Suterwala Shabbir
- Svensson Fredrik
- Sverzhinsky Aleksandr
- Swart Tarryn
- Taglialatela Angelo
- Tam Heng-Keat
- Tandon Vasudha
- Tang Weiping
- Tang Young
- Tanner John J.
- Taylor Richard E.
- Teixeira Thaiz Rodrigues
- Teramoto Tadahisa
- Thai Van Chi
- Thayer Desiree
- Thomas Bill
- Thompson Erik W.
- Tilford Hannah
- Tiwari Rakesh Kumar
- Toh Alan Kie Leong
- Tomilov Alexey
- Toogood Peter
- Torner Carles
- Trabocchi Andrea
- Trader Darci J.
- Trakhtenberg Ephraim F.
- Trinh Nguyen Mai
- Truong Ha
- Tse-Dinh Yuk-Ching
- Tsimbalyuk Sofiya
- Tumes Damon J.
- Tye Mark A.
- Uribe Ruben Vazquez
- Valli Marilia
- van den Akker Focco
- van den Bedem Henry
- Van Doren Steven R.
- Van Grack Tessa
- Van Hung Le Vuong
- Van Pelt Natascha
- Van Remmen Holly
- Van Voorhis Wesley C.
- Vandenberg Robert J.
- Veit Guido
- Verhamme Ingrid M.
- Verma Rajkumar
- Viola Ronald E.
- Virtanen Anniina
- Vizeacoumar Franco J.
- Vizeacoumar Frederick S.
- Vleminckx Margot
- von Hundelshausen Philipp
- Voss Jan Hendrik
- Vrielink Alice
- Waggoner Stephen N.
- Walensky Loren D.
- Wallach Izhar
- Wang Feng
- Wang Jianghai
- Wang Jun
- Wang Xingyou
- Wang Zhenghe
- Warrington Jeffrey M.
- Watkins Joshua
- Wazir Sarah
- Weber Christian
- Welsbie Derek S.
- Wentworth Kelly L.
- Wert-Lamas Leon
- White Andrew
- White Simon J.
- Whitesell Luke
- Williams Tiffany
- Wilson Cornelia M.
- Wilson Mark A.
- Windisch Marc P.
- Wong Keith S.
- Woods Virgil A.
- Worley Brad
- Wu Pengpeng
- Wu Xiaoyang
- Wulff Heike
- Xiang Fei
- Xu Hongyang
- Xu Jiake
- Xu Jingyi
- Xu Sophia Q.
- Xu Xin
- Yan Riqiang
- Yang Chao-Yie
- Yen Yun
- Young Matthew A.
- Yu Fang
- Yu Xinfang
- Yuan Haynes
- Yuan Xinrui
- Zahler Stefan
- Zeina Christina M.
- Zelinskaya Natalia
- Zhang Dingqiang
- Zhang Gang
- Zhang Wenjun
- Zhang Xu
- Zhang Yan Jessie
- Zhang Zhiguo
- Zhao Jinshi
- Zhou Han
- Zhou Hui
- Zhou Jia
- Zhou Pei
- Zhou Shan
- Zhu Jiaqi
- Zhu Siran
- Zhu Yini
- Zhuo Ling
- Zochodne Douglas William
- Publication venue
- Publication date
- 01/01/2024
- Field of study
: High throughput screening (HTS) is routinely used to identify bioactive small molecules. This requires physical compounds, which limits coverage of accessible chemical space. Computational approaches combined with vast on-demand chemical libraries can access far greater chemical space, provided that the predictive accuracy is sufficient to identify useful molecules. Through the largest and most diverse virtual HTS campaign reported to date, comprising 318 individual projects, we demonstrate that our AtomNet® convolutional neural network successfully finds novel hits across every major therapeutic area and protein class. We address historical limitations of computational screening by demonstrating success for target proteins without known binders, high-quality X-ray crystal structures, or manual cherry-picking of compounds. We show that the molecules selected by the AtomNet® model are novel drug-like scaffolds rather than minor modifications to known bioactive compounds. Our empirical results suggest that computational methods can substantially replace HTS as the first step of small-molecule drug discovery
Genetic mechanisms of critical illness in COVID-19.
- Author
- A A Roger Thompson
- A Abraheem
- A Agasou
- A Ahmed
- A Ali
- A Allan
- A Altabaibeh
- A Alvaro
- A Aspinwall
- A Ayers
- A Bamford
- A Barron
- A Bashyal
- A Bellini
- A Bociek
- A Botello
- A Bowes
- A Brady
- A Brayne
- A Brown
- A Brown
- A Butler
- A Campbell
- A Carter
- A Collins
- A Cowley
- A Cowton
- A Cowton
- A Cox
- A Crew
- A Dance
- A Daniel
- A Daniels
- A Dela Rosa
- A Drummond
- A Durie
- A E Heron
- A Easthope
- A Easthope
- A Evans
- A Fofano
- A Gales
- A Ganesan
- A Gardner
- A Garg
- A Gherman
- A Gordon
- A Gratrix
- A Gulati
- A Gupta
- A Haigh
- A Haldeos
- A Harrison
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- A Higham
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- A Knight
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- A Kuravi
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- A McGregor
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- A Rattray
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- A Reed
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- A Rose
- A Rose
- A Rostron
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- A Roynon-Reed
- A S Raj
- A Salberg
- A Sanderson
- A Serrano-Ruiz
- A Solesbury
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- A Swain
- A Tariq
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- A Zak
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- Achille Iolascon
- Adam Auton
- Adam Brown
- Agnese Verzuri
- Agostino Ognibene
- Agostino Riva
- Ailsa Golightly
- Alan Maclean
- Alessandra
- Alessandra Stella
- Alessandra Vergori
- Alessia Giorli
- Alexander J Mentzer
- Alice Donati
- Alison M Meynert
- Alistair Nichol
- Ana da Silva Filipe
- Andrea Antinori
- Andrea Cossarizza
- Andrea Ganna
- Andrea Tommasi
- Andrew Rambaut
- Andrew Stenhouse
- Andy Law
- Anjali J Shastri
- Anna Canaccini
- Anna Maria Pinto
- Annarita Giliberti
- Annemarie B Docherty
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- Bruno Frediani
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- Samreen Ijaz
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- Stephanie Roberts
- Stephen R Knight
- Summers Charlotte
- Susanna Croci
- Susanna Guerrini
- T Anderson
- T Arden
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- T O Jones
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- Tammy Gilchrist
- Tenesa Albert
- Teresa Filshtein-Sonmez
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- Thushan de Silva
- Tim Walsh
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- Tony Wackett
- Trevor Paterson
- Tullio Trotta
- Turtle Lance
- U Poultney
- V Amin
- V Anumakonda
- V Bastion
- V Cannons
- V Crickmore
- V Gopal
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- Valentina Anemoli
- Vanessa Sancho-Shimizu
- Victoria Shaw
- Vitart Veronique
- W Harrison
- W Khaliq
- W Khaliq
- W McCormick
- W Woodyatt
- Walker Susan
- Walsh Timothy
- Wang Bo
- Wei Shen Lim
- Wendy S Barclay
- William A Paxton
- William Greenhalf
- Wilson James F
- Wrobel Nicola
- Wu Yang
- X Qiu
- Y Baird
- Y Choudhury
- Y Hussain
- Y Jackson
- Y Thirlwall
- Yang Jian
- Yang Zhijian
- Z Alldis
- Z Belagodu
- Z Bradshaw
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- Z Daly
- Z Farzad
- Z Fernandez
- Z Garland
- Z Maqsood
- Z Omar
- Z Prime
- Z Scott
- Zechner Marie
- Zhai Ranran
- Zheng Chenqing
- Publication venue
- Nature
- Publication date
- 01/01/2020
- Field of study
Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 × 10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice
Whole-genome sequencing reveals host factors underlying critical COVID-19
- Author
- Abd Elghafar M. S.
- Abdel-Aziz M.
- Abdelrazik M.
- Abdollahi H.
- Abdullah T.
- Abecasis G. R.
- Abedalthagafi M.
- Abel L.
- Abernathy C.
- Abraheem A.
- Abul-Husn N. S.
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- Adanini O.
- Adeleye O.
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- Afilalo J.
- Afilalo M.
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- Aksentijevich A.
- Al-Afghani H.
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- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
Whole-genome sequencing reveals host factors underlying critical COVID-19
- Author
- Abd Elghafar M.S.
- Abdel-Aziz M.
- Abdelrazik M.
- Abdollahi H.
- Abdullah T.
- Abecasis G.R.
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- Zöllner S.
- Åsvold B.O.
- Publication venue
- Springer Science and Business Media LLC
- Publication date
- 07/07/2022
- Field of study
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease