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Evaluating the Effectiveness of Interventions to Improve the Follow-up Rate for Children With Visual Disabilities in an Eye Hospital in Nepal: Nonrandomized Study

Author: Agiwal Varun
Ale Daman
Bhandari Gopal
Byanju Raghunandan
Chaudhary Daya Shankar
Ghimire Ramesh
Gudlavalleti Anirudh Gaurang
Kamalakannan Sureshkumar
Karki Rakshya
Kayastha Sajani
Murthy Gudlavalleti Venkata Satyanarayana
Operational Research Capacity Building Study Group
Pandey Binod
Pant Hira
Rathi Suresh Kumar
Shrestha Manisha
Publication venue: 'JMIR Publications Inc.'
Publication date: 23/02/2023
Field of study

Background: Monitoring ocular morbidity among pediatric patients requires regular follow-up visits. We found that the follow-up rate was poor among children in our setting. Therefore, we intended to assess the effectiveness of 2 interventions—(1) counseling and (2) SMS text messaging and phone calls—to improve the follow-up rates. Objective: This study aimed to evaluate the effectiveness of 2 interventions, counseling and SMS and phone calls group, as well as a routine standard care for improving the follow-up rate of pediatric patients. Methods: A Nonrandomized, quasiexperimental design was used. Children (aged 0-16 years) with ocular conditions requiring at least 3 follow-up visits during the study period were included. A total of 264 participants were equally allocated to the 3 intervention groups of (1) counseling, (2) SMS and phone calls, and (3) routine standard care group. A 20-minute counseling session by a trained counselor with the provision of disease-specific leaflets were given to those in the counseling group. For the second intervention group, parents of children received an SMS text 3 days before and a phone call 1 day before their scheduled follow-up visits. Participants allocated for the routine standard care group were provided with the existing services with no additional counseling and reminders. Participants attending 3 follow-ups within 2 days of the scheduled visit date were considered compliant. The difference in and among the proportion of participants completing all 3 follow-up visits in each group was assessed. Results: The demographic characteristics of the participants were similar across the study groups. Only 3% (8/264) of participants completed all 3 follow-up visits, but overall compliance with the follow-up, as defined by the investigators, was found to be only 0.76% (2/264). There was no statistically significant difference in the proportion of follow-up between the intervention groups. However, the proportion of participants attending the first and second follow-ups, as well as the overall total number of follow-ups, was more in the SMS and phone-call group followed by the counseling group. Conclusions: We did not find any evidence on the effectiveness of our interventions to improve the follow-up rate. The primary reason could be that this study was conducted during the COVID-19 pandemic. It could also be possible that the intensity of the interventions may have influenced the outcomes. A rigorously designed study during the absence of any lockdown restrictions is warranted to evaluate intervention effectiveness. The study also provides useful insights and highlights the importance of designing and systematically developing interventions for improving the follow-up rate and ensuring a continuum of care to children with visual disabilities in Nepal and similar contexts. Trial Registration: ClinicalTrials.gov NCT04837534; https://clinicaltrials.gov/ct2/show/NCT04837534 International Registered Report Identifier (IRRID): RR2-10.2196/3157

Northumbria University Research Portal

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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.
Acquilini D.
Adams C.
Adams E. L.
Adams K.
Adamsara A.
Adanini O.
Adeleye O.
Adra D.
Afilalo J.
Afilalo M.
Afolabi D.
Afrasiabi Z.
Agasou A.
Agrawal S.
Aguero D.
Ahmad N.
Ahmadi S.
Ahmed A.
Ahmed C.
Akeroyd L.
Akhtar M. N.
Akinkugbe O.
Aksentijevich A.
Al-Afghani H.
Al-Awdah L.
Alaamery M.
Alahmadey Z. Z.
Alaverdian D.
Alavere H.
Albader A.
Albaiceta G. M.
Albakri J. K.
AlBardis H.
Albeladi M.
Albesher N.
Albrich W.
AlDhawi N.
Aldridge J.
Aleagha A. E.
Alexander P.
Alfonso J.
Alghamdi B.
Alghamdi J.
Ali A.
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Wulandari R.
Wyllie D. H.
Wynter I.
Xavier K.
Xue X.
Yadav A.
Yang J.
Yassen A. M.
Yates B.
Ye C.
Yun N.
Zainy T.
Zak A.
Zaki A.
Zamikula J.
Zanella I.
Zborowski A. C.
Zeberg H.
Zechner M.
Zguro K.
Zhang M.
Zhao J. H.
Zheng C.
Zhou W.
Zitter L.
Zlatopolsky M.
Zollner S.
Zongo O.
Zucchi P.
Zyndorf M.
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

PubliCatt

Archivio istituzionale della ricerca - Università di Modena e Reggio Emilia

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.
Abecasis G.R.
Abedalthagafi M.
Abel L.
Abernathy C.
Abraheem A.
Abul-Husn N.S.
Acquilini D.
Adams C.
Adams E.L.
Adams K.
Adamsara A.
Adanini O.
Adeleye O.
Adra D.
Afilalo J.
Afilalo M.
Afolabi D.
Afrasiabi Z.
Agasou A.
Agrawal S.
Agüero D.
Ahmad N.
Ahmadi S.
Ahmed A.
Ahmed C.
Akeroyd L.
Akhtar M.N.
Akinkugbe O.
Aksentijevich A.
Al Harthi F.
Al Mutairi A.
Al-Afghani H.
Al-Awdah L.
Alaamery M.
Alahmadey Z.Z.
Alaverdian D.
Alavere H.
Albader A.
Albaiceta G.M.
Albakri J.K.
AlBardis H.
Albeladi M.
Albesher N.
Albrich W.
AlDhawi N.
Aldridge J.
Aleagha A.E.
Alexander P.
Alfonso J.
Alghamdi B.
Alghamdi J.
Ali A.
Ali A.
Ali I.A.M.
Ali S.
Aliannejad R.
Aljawini N.
AlJohani S.
Alkwai S.
Allan A.
Allan E.
Allan J.
Alldis Z.
Allen L.
Allen M.
Allen S.
Allibone S.
Allison K.S.
Allos R.
Almaden-Boyle C.
AlMalik A.
Almalki F.
Almohammed I.
Almutairi M.
Alotaibi S.
Alowayn A.M.
Alqahtani S.
Alqubaishi F.
Alrashed M.
Alshareef A.
Alsolm E.
Alswailm M.
Altabaibeh A.
Alvaro A.
AlZahrani D.
Amin V.
Amirsavadkouhi A.
Amitrano S.
Anastasescu E.
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Anderson J.
Anderson M.
Anderson P.
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Anderson T.
Andolfo I.
Andretta F.
Andreucci E.
Andrew A.
Andrew B.
Andrew G.
Andrews E.
Andrews S.J.
Anedda F.
Anemoli V.
Annis A.
Antcliffe D.
Antinori A.
Antoni M.D.
Anumakonda V.
Apetri E.
Aquino M.
Arabi Y.M.
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Wild L.
Wild L.
Wilding L.
Wiles M.
Wilkins J.
Wilkinson A.
Wilkinson B.
Willer C.
Williams A.
Williams A.
Williams A.
Williams A.T.
Williams D.
Williams E.
Williams F.
Williams G.
Williams H.
Williams K.
Williams M.
Williams P.
Williams S.
Williams T.
Willis C.
Willis H.
Wills M.
Willson J.
Wilson A.
Wilson D.J.
Wilson J.
Wilson J.F.
Wilson J.F.
Winnard S.
Winter-Goodwin B.
Wolf-Roberts R.
Wolford B.
Wong J.
Wood D.
Wood H.-L.
Wood S.
Wood T.
Woodford C.
Woodruff M.
Woods L.
Woodyatt W.
Woolley A.E.
Worner R.
Worsley L.
Wray G.
Wren L.
Wrey Brown C.
Wright D.
Wright J.
Wright M.
Wrobel N.
Wu Y.
Wulandari R.
Wyllie D.H.
Wynter I.
Xavier K.
Xue X.
Yadav A.
Yang J.
Yassen A.M.
Yates B.
Ye C.
Yun N.
Zainy T.
Zak A.
Zaki A.
Zamikula J.
Zanella I.
Zborowski A.C.
Zeberg H.
Zechner M.
Zechner M.
Zguro K.
Zhang M.
Zhao J.H.
Zheng C.
Zhou W.
Zitter L.
Zlatopolsky M.
Zongo O.
Zucchi P.
Zyndorf M.
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

White Rose Research Online

Improving the Follow-up Rate for Pediatric Patients (0-16 years) of an Eye Hospital in Nepal: Protocol for a Public Health Intervention Study

Author: Anirudh Gaurang Gudlavalleti
Binod Pandey
Daman Ale
Daya Shankar Chaudhary
Gopal Bhandari
Manisha Shrestha
Raghunandan Byanju
Ramesh Ghimire
Sajani Kayastha
Suresh Kumar Rathi
Publication venue: JMIR Publications
Publication date: 01/10/2021
Field of study

BackgroundThe follow-up of pediatric patients ensures regular ocular morbidity monitoring and better treatment outcome. Hiralal Santudevi Pradhan Institute of Ophthalmic Science (Bharatpur Eye Hospital [BEH]) noticed that the follow-up rate was only 22% among its pediatric patients. Several factors like lack of awareness and forgetfulness among patients may contribute to a lower number of follow-up visits. Therefore, BEH decided to find if counseling and reminders through SMS text messaging and phone calls would improve the follow-up rates. ObjectiveThis study aims to evaluate the impact of interventions like counseling and reminder SMS text messaging and phone calls in improving the follow-up rate of pediatric patients. MethodsThis is a public health intervention study being conducted using quantitative analysis. All children (0-16 years) with ocular conditions requiring at least 3 follow-up visits in the study period will be included. In all, 264 participants will be allocated to 3 groups: routine standard care, counseling, and reminders with SMS text messaging and phone calls. In counseling, patients will take part in 20-minute counseling sessions with trained counselors at each visit, and information leaflets will be provided to them. In the reminder SMS text messaging and phone call group, patients will receive an SMS text message 3 days prior and a phone call 1 day prior to their scheduled visits. Patients attending within 2 days of the scheduled date will be considered compliant to follow-up. The proportion of patients completing all the follow-up visits in each group will be assessed. Informed consent will be taken from parents and children. Univariate and multivariate analyses will be conducted. ResultsThe ethical approval for this study has been obtained from the Ethical Review Board (ERB) of Nepal Health Research Council (ERB protocol registration #761/2020 P). The data collection was initiated on January, 24, 2021, but due to the COVID-19 pandemic, as of September 2021, we have only been able to enroll 154 of the planned 264 participants (58.3% of the sample size). ConclusionsThis study will reliably document not only the factors associated with follow-up rate through an intervention package (counseling and reminders through SMS text messaging and phone calls) but also the cost effectiveness of the intervention package, which can be applied in all the departments of the hospital. Trial RegistrationClinicalTrials.gov NCT04837534; https://clinicaltrials.gov/ct2/show/NCT04837534 International Registered Report Identifier (IRRID)DERR1-10.2196/3157

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Village-integrated eye workers for prevention of corneal ulcers in Nepal (VIEW study): a cluster-randomised controlled trial

Author: Acharya Nisha R
Adhikari Manmohan
Basset Ken
Bhandari Gopal
Bhandari Sadhan
Bhattarai Dipak
Bhattarai Rabin
Bista Dikshya
Byanju Raghunandan
Byanju Raghunandan
Chapagain Dipak
Chase Heidi
Chaudhary Ajay Kumar
Chaudhary Daya Shankar
Choudhary Shravan
Cotter Sun Y
Dahal Gokul
Dhakwa Parami
Evans Lauren
Fletcher Daniel A
Gautam Mariya
Gautam Shree Krishna
Ghimire Ramesh
Gilbert Suzanne
Giri Gaurav
Giri Puspa
Gonzales John A
Gonzales John A
Group Village-Integrated Eye Worker Trial
Gurau Dhanmaya
Gurung Jeevan
Hamal Vivek
Kandel Deepak
Kandel Ram P
Kandel Ram Prasad
Kayastha Sajani
Keenan Jeremy D
Keenan Jeremy D
Khadka Kamal Bahadur
Kim Jessica
Lamichhane Pradip Chandara
Lee Salena
Lietman Thomas M
Lietman Thomas M
Maamari Robi N
McLeod Stephen D
Moses Deborah
O'Brien Kieran S
O’Brien Kieran S
Parajuli Tulsi Prasad
Porco Travis C
Porco Travis C
Poudyal Bimal
Poudyal Bimal
Ramirez David A
Ray Kathryn J
Reber Clay D
Rijal Rajendra
Rose-Nussbaumer Jennifer
Shah Ranjeet Kumar
Sharma Niraj
Sharma Prafulla
Shrestha Anju
Shrestha Manisha
Srinivasan Muthiah
Srinivasan Muthiah
Subedi Pradeep
Tenzing Chundak
Upadhyay Madan
Upadhyay Madan
Whitcher John P
Whitcher John P
Publication venue: eScholarship, University of California
Publication date: 01/04/2022
Field of study

BackgroundCorneal ulcers are a common cause of blindness in low-income and middle-income countries, usually resulting from traumatic corneal abrasions during agricultural work. Antimicrobial prophylaxis of corneal abrasions can help prevent corneal ulcers, but delays in the initiation of therapy are frequent. We aimed to assess whether a community-based programme for corneal ulcer prevention would reduce the incidence of corneal ulceration.MethodsA cluster-randomised trial was performed in village development committees (VDCs) in Nepal. VDCs in the catchment area of Bharatpur Eye Hospital, Nepal with less than 15 000 people were eligible for inclusion. We randomly assigned (1:1) VDCs to either an intervention group or a control group. In the intervention VDCs, existing female community health volunteers (FCHVs) were trained to diagnose corneal abrasions and provide a 3-day course of ophthalmic antimicrobials to their patients. In the control VDCs, FCHVs did not provide this intervention. Participants were not masked given the nature of the intervention. Both groups were followed up for 3 years for photographic evidence of corneal ulceration. The primary outcome was the incidence of corneal ulceration, determined by masked assessment of corneal photographs. The analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, NCT01969786.FindingsWe assessed 112 VDCs, of which 24 were enrolled. The study was performed between Feb 4, 2014, and Oct 20, 2017. 12 VDCs were randomly assigned to the intervention group and 12 to the control group. 252 539 individuals were included in the study (130 579 in the intervention group and 121 960 in the control group). FCHVs diagnosed and provided antimicrobials for 4777 corneal abrasions. The census identified 289 corneal ulcers among 246 893 person-years in the intervention group (incidence 1·21 cases [95% CI 0·85-1·74] per 1000 person-years) and 262 corneal ulcers among 239 170 person-years in the control group (incidence 1·18 cases [0·82-1·70] per 1000 person-years; incidence rate ratio 1·03 [95% CI 0·63-1·67]; p=0·93). Medication allergy was self-reported in 0·2% of participants.InterpretationWe did not detect a reduction in the incidence of corneal ulceration during the first 3 years of a community-based corneal ulcer prevention programme. Further study might be warranted in more rural areas where basic eye care facilities are not available.FundingNational Eye Institute

eScholarship - University of California

Sarcocystis and sarcocystosis in India: status and emerging perspectives

Author: A Kumar
A Prakash
A Saleque
A Saleque
A Saleque
A Saleque
A Vasudevan
AK Jain
AK Saha
AK Saha
AM Dafedar
AS Naidu
AV Deshpande
AV Deshpande
AV Deshpande
BA Pandit
BA Pandit
BB Bhatia
BB Singh
BMA Latif
BN Mohanty
BN Mohanty
BN Sahai
BN Sahai
CM Brown
CP Swarnkar
Daya Shankar
DK Pethkar
G Rao
G Shrivastava
GS Mamatha
Hema Prasanth
Hema Prasanth
HL Shah
HN Achuthan
HN Achuthan
HS Gill
JP Dubey
JP Dubey
JP Dubey
JP Dubey
K Rohini
K Srinivasa Rao
K Srinivasa Rao
KP Singh
KP Singh
KP Singh
KP Singh
L Singh
LM Gonzalez
MB Chhabra
MB Chhabra
MM Hussain
NC Patra
OK Gupta
PC Jain
PC Jain
PC Jain
PC Jain
PC Jain
PD Jumde
PD Juyal
PD Juyal
PD Juyal
PD Juyal
PD Juyal
PD Juyal
PD Juyal
PD Juyal
PD Juyal
PD Juyal
PD Juyal
PK Agarwal
PK Chaudhary
PK Solanki
PK Solanki
PK Solanki
PK Solanki
PK Solanki
PP Devi
PPS Chauhan
PS Banerjee
PS Banerjee
PS Srivastava
R Venu
R Venu
RK Agnihotri
RK Chaudhary
RK Chaudhary
RK Sharma
RS Aulakh
RS Avapal
RS Avapal
RS Avapal
RS Avapal
S Dey
SB Ghoshal
SB Ghoshal
SB Ghoshal
SB Ghoshal
SC Gupta
SL Gupta
SL Gupta
SL Gupta
SV Wadajkar
SV Wadajkar
UV Shastri
UV Shastri
Publication venue: 'Springer Science and Business Media LLC'
Publication date
Field of study

Crossref

Mapping the human genetic architecture of COVID-19

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Abdullah T.
Abe R.
Abe S.
Abecasis G. R.
Abel L.
Abernathy C.
Abraheem A.
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Akinkugbe O.
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Al Thani A.
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Publication venue: 'Springer Science and Business Media LLC'
Publication date: 01/01/2021
Field of study

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease

Archivio istituzionale della ricerca - Politecnico di Milano

Archivio della ricerca - Università degli studi di Napoli Federico II

Archivio della Ricerca - Università degli Studi di Siena

Archivio istituzionale della ricerca - Alma Mater Studiorum Università di Bologna

Archivio istituzionale della ricerca - Università di Genova

UTUPub

Archivio istituzionale della ricerca - Università di Modena e Reggio Emilia

Archivio istituzionale della ricerca - Università di Padova

Whole-genome sequencing reveals host factors underlying critical COVID-19

Author: Abd Elghafar Mohamed S.
Abdel-Aziz Mahmoud
Abdelrazik Marwa
Abdollahi Hamed
Abdullah T.
Abecasis Goncalo
Abedalthagafi M.
Abel Lynn
Abernathy C.
Abraheem Azmeralde
Abul-Husn Noura S.
Acquilini D.
Adams C.
Adams Emma L.
Adams K.
Adamsara Alireza
Adanini Olurenke
Adeleye O.
Adra D.
Afilalo J.
Afilalo M.
Afolabi D.
Afrasiabi Z.
Agasou A.
Agrawal Shruti
Agüero D.
Ahmad N.
Ahmadi Saeideh
Ahmed A.
Ahmed Cecilia
Akeroyd L.
Akhtar M.N.
Akinkugbe O.
Aksentijevich Alexandra
Al-Afghani H.
Al-Awdah L.
Alaamery M.
Alahmadey Z.Z.
Alaverdian D.
Alavere H.
Albader A.
Albaiceta G.M.
Albakri J.K.
AlBardis H.
Albeladi M.
Albesher N.
Albrich W.
AlDhawi N.
Aldridge J.
Aleagha Afshar Etemadi
Alexander Peter.
Alfonso J.
Alghamdi B.
Alghamdi J.
Ali A.
Ali Altaf
Ali I.A.M.
Ali Syamlan
Aliannejad Rasoul
Aljawini N.
AlJohani S.
Alkwai S.
Allan A.
Allan E.
Allan J.
Alldis Zoe
Allen L.
Allen Meryem
Allen Schvearn
Allibone S.
Allison K.S.
Allos R.
Ally S.M.
AlMalik A.
Almalki F.
Almohammed I.
Almutairi M.
Alotaibi S.
Alowayn A.M.
Alqahtani S.
Alqubaishi F.
Alrashed M.
Alshareef A.
Alsolm E.
Alswailm M.
Altabaibeh A.
Alvaro A.
AlZahrani D.
Amin V.
Amirsavadkouhi Ali
Amitrano Sara
Anastasescu E.
Anderson F.
Anderson J.
Anderson Madeleine
Anderson Peter
Anderson S.
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Anderson T.
Andolfo I.
Andretta F.
Andreucci E.
Andrew Angela
Andrew B.
Andrew Gratrix
Andrews E.
Andrews Shea J.
Anedda F.
Anemoli V.
Annis A.
Antcliffe David
Antinori Andrea
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Anumakonda V.
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Aquino Maia
Arabi Y.M.
Aravindan Latha
Arbane Gill
Archer Katie
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Arias Sonia Sousa
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Zheng Chenqing
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Zlatopolsky Menachem
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Zyndorf Marissa
Zöllner S.
Åsvold Bjørn Olav
Publication venue
Publication date: 01/01/2022
Field of study

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization 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

Diposit Digital de Documents de la UAB

Mapping the human genetic architecture of COVID-19

Author: Abdelrazik M
Abdullah T
Abe R
Abe S
Abecasis GR
Abel L
Abernathy C
Abraheem A
Abul-Husn NS
Acosta-Herrera M
Acquilini D
Acquilini D
Adachi T
Adachi Y
Adams C
Adams K
Adanini O
Adeleye O
Adeniji K
Adra D
Afifi N
Afilalo J
Afilalo M
Afolabi D
Afrasiabi Z
Afset JE
Agasou A
Aghemo A
Agranoff D
Agrawal S
Aguirre LA
Agwuh K
Ahmad HF
Ahmad N
Ahmed A
Ahmed C
Ahmed KA
Ai M
Ail D
Akeroyd L
Akhtar MN
Akhtar S
Akinkugbe O
Aksentijevich A
Al Thani A
Al-Muftah W
Al-Sarraj Y
Alarcon C
Alarcon-Riquelme ME
Alasdair F
Alaverdian D
Alavere H
Albertos R
Albillos A
Albrecht W
Albrich W
Albrich WC
Aldera EL
Aldridge J
Alegria A
Alex B
Alexander P
Alfonso J
Algera AG
Ali A
Ali IMA
Ali S
Aliberti S
Allan A
Allan E
Allan J
Alldis Z
Allen L
Allen S
Allibone S
Allison KS
Allos R
Ally SM
Almaden-Boyle C
Altabaibeh A
Altmueller J
Alvaro A
Amar D
Amin V
Amitrano S
Amiya S
Ampuero J
Anan R
Anania S
Anastasescu E
Anderson F
Anderson J
Anderson M
Anderson P
Anderson S
Anderson S
Anderson T
Ando A
Andolfo I
Andrade V
Andretta F
Andreucci E
Andreucci E
Andrew A
Andrew B
Andrew G
Andrews E
Andrews SJ
Andrews SJ
Andrews SJ
Andrews SJ
Andrikopoulos P
Anedda F
Aneli S
Anemoli V
Angelini C
Angus B
Annis A
Antcliffe D
Antinori A
Antoni MD
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Delaneau O
Delgado CC
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Fernandez J
Fernandez Z
Fernandez-Cadenas I
Fernandez-Cadenas I
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Fernandez-Roman J
Ferrando C
Ferreira MAR
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Ferwerda B
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Filipe ADS
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Finney C
Finucane H
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Fiorentino G
Fisher E
Fisher LWS
Flaherty L
Flanagan R
Fletcher T
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Flint N
Foco L
Fofano A
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Force HCT
Ford A
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Galvan-Femenia I
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Garcia-Dorival I
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Goldstein DB
Goldstein JI
Golightly A
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Gomez-Cabrero D
Gon Y
Gondo P
Gonzalez Cejudo T
Goodchild D
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Griffin JL
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Grp NS-CS
Grzymski JJ
Gualtierotti R
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Moore E
Moore F
Moore KHS
Moore LSP
Moore SC
Moore SC
Moore SC
Mooser V
Moreira L
Moreno D
Moreno V
Moreno V
Moreno-Cuesta J
Moreno-Estrada A
Morgan A
Morgan J
Morgan P
Mori N
Morilla R
Morino E
Morisaki H
Morita A
Morrice K
Morrice K
Morris A
Morris C
Morris L
Morris S
Morrison A
Morrison DR
Mortimore K
Moses S
Moss S
Mostoles L
Motegi M
Motherwell N
Moultrie S
Moutschen M
Moutsianas L
Moutsianas L
Moya L
Mpenge M
Msiska M
Mtuwa S
Muchenje N
Mueller F
Mueller KE
Mulcahy M
Mulla R
Mulla S
Mullan D
Mullan D
Muniz-Diaz E
Munt S
Munting A
Mupudzi M
Murakami K
Murdoch E
Murdoch S
Murohashi K
Murphy A
Murphy C
Murphy D
Murphy EG
Murphy L
Murphy L
Murphy L
Murphy M
Murphy SN
Muscatello A
Mussini C
Mutch R
Mutoh Y
Mwaura E
Mwaura L
My I
Myhre R
Naaber P
Nadkarni GN
Nafria-Jimenez B
Nagai H
Nagarajan T
Nagasaki T
Nagasaki Y
Nagata K
Nagel M
Nagra I
Naisbitt J
Nakachi I
Nakada T-A
Nakajima J
Nakajima Y
Nakamura A
Nakamura M
Nakamura Y
Nakanishi T
Nakanishi T
Nakanishi T
Nakanishi T
Nakano S
Nakano Y
Nakayama S
Namkoong H
Nandakumar R
Nanki K
Nannya Y
Naranjo A
Narita A
Narumoto O
Nasir F
Nasir J
Navas E
Nayak M
Naylor S
Nazari R
Neal A
Neale BM
Neale BM
Neb H
Nebel A
Negro TR
Nellen J
Nelson M
Nencioni C
Neofytos D
Neofytos D
Netherton K
Neveux I
Newell H
Newey L
Newman B
Newman J
Newman J
Newman T
Newton M
Ng A
Nguyen H
Nguyen H
Niblo K
Nichol A
Nichol A
Nicholson A
Nicholson A
Nicholson A
Nickle D
Nicol L
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Niemi MEK
Niemi MEK
Niemi MEK
Niemi MEK
Niemi MEK
Niemi MEK
Nieto R
Nii T
Niitsu T
Nikitas N
Nilsson A
Nishi K
Nishio K
Nishitsuji M
Nishiyama K
Nishiyama K
Nivard MG
Niwa K
Nixon R
Nkambule L
Nkambule L
Nkambule L
Nkambule L
Nkambule L
Noble H
Noda J
Noda Y
Noethen MM
Nolan C
Norddahl G
Norman K
Norman L
Norris J
Nortcliffe T
North J
Nossent EJ
Noto K
Noursadeghi M
Novis C
Nussle SG
Nussle SG
Nutescu E
Nwafor L
O'Brien L
O'Brien P
O'Brien T
O'Byrne SM
O'Connell AM
O'Connell J
O'Connell S
O'Connor G
O'Donnell CJ
O'Donnell P
O'Hara M
O'Keefe L
O'Leary K
O'Leary R
O'Mahony L
O'Malley L
O'Neil P
O'Neill L
O'Reilly K
O'Reilly P
O'Shea MK
O'Sullivan S
Oakley N
Obeidat M
Oblak M
Odam M
Odani T
Oddo M
Odhams CA
Oezer O
Ogata T
Ogawa S
Ogawa S
Ogg B
Ognibene A
Oguma T
Ogura S
Ogura T
Ohba T
Ohta S
Okada T
Okada Y
Okada Y
Okamori S
Okamoto M
Olanipekun M
Oliveira M
Olufuwa O
Omae Y
Omar Z
Omodei P
Ono A
Onoi K
Ooshima N
Oosthuyzen W
Openshaw PJM
Ori APS
Ortiz AB
Osagie A
Ostadreza M
Ostermann M
Ostermann M
Otahal I
Otahal I
Otahal I
Oxspring S
Oyamada Y
Ozaki S
P-PredictUs
Paccapelo C
Paciosi F
Paciosi F
Paciosi F
Packham S
Padden G
Pagani JL
Pagani JL
Page VJ
Paik N-J
Pairo-Castineira E
Pais M
Palmarini M
Palmer DS
Palmieri C
Palmieri M
Palmieri O
Palom A
Palotie A
Palotie A
Panchatsharam S
Pancrazi A
Panese S
Pantet O
Papakonstantinou D
Papineni P
Pappa E
Paraboschi EM
Paraiso H
Paramsothy R
Parati G
Parikh V
Parisi SG
Park D
Park JS
Park KU
Park L
Park S-K
Park WB
Parker R
Parkin J
Parkinson N
Parkinson N
Parkinson P
Parmar C
Parravicini P
Parris V
Parris V
Parsons P
Partha R
Partridge R
Parzibut G
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Pasaniuc B
Pascual-Iglesias A
Pasko D
Pasko D
Pasko D
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Patel B
Patel B
Patel BV
Patel K
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Patel S
Patel T
Paterson T
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Pathak GA
Pathak GA
Pathan N
Pattaro C
Pattaro C
Pattison N
Pattison N
Paul P
Paulus F
Pavlovic M
Paxton WA
Pazos MDLM
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Pearson NM
Pearson S
Peasgood E
Peasgood E
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Peloso G
Pelusi S
Penacerrada M
Pendergrass S
Pendlebury J
Pendrick D
Penn R
Penrice-Randal R
Pepperell J
Peree H
Pereira AC
Perera M
Perez EF
Perez J
Perez-Tur J
Perez-Tur J
Perkins E
Perna R
Perola M
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Perret A
Perry J
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Perticaroli V
Peruggia M
Perumal S
Peschuck A
Pesenti A
Pessina G
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Pesukova J
Peter W
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Peters E
Peters M
Peters MJ
Peterson P
Petitjean L
Petrocelli P
Petrocelli P
Petty LE
Peyrassol X
Peyvandi F
Pezzoli G
Pheby J
Philbin J
Phillips C
Phillips C
Phillips P
Phipps J
Phull M
Phull M
Piacentini P
Picchiotti N
Pichon B
Pickard A
Piercy C
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Pigazzini S
Pigazzini S
Pigazzini S
Pigazzini S
Pilgrim J
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Pinksy B
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Pinto AM
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Pinzuti I
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Piscopo C
Pitts S
Pius R
Player B
Plotnikov N
Pogreban T
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Polgar O
Polgarova P
Polikowsky HG
Polimanti R
Pollakis G
Pollard R
Poller W
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Ponting CP
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Pooni JS
Popescu M
Popov I
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Portopena L
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Pothecary C
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Potoczna D
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Poulaka M
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Price R
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Protzer U
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Prout R
Prout R
Prysyazhna O
Pugh R
Pugin J
Pumarola T
Purewal M
Purohit D
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Puusepp M
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Puxty K
Pye K
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Quaid S
Queiroz J
Quereda C
Quinn A
Quinn H
Quinodoz M
Quinodoz M
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Raasveld J
Rad L
Rader D
Radermecker C
Radford E
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Raffat N
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Rahier J-F
Rahmouni S
Rahmouni S
Rahmouni S
Rai SG
Raimondi F
Raith E
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Raithatha A
Raj M
Raja A
Rakitko A
Rambaut A
Ramirez A
Ramos L
Rancan I
Rand J
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Randell G
Rando-Segura A
Rangarajan H
Rankin T
Ratnam V
Rattray A
Ravaglia S
Rawlik K
Rawlins J
Ray S
Raychaudhuri S
Raynard D
Reddy A
Reece-Anthony R
Reed A
Rees A
Rees S
Rees T
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Regina J
Rehman H
Reid K
Reijnders T
Reilly MP
Reimann E
Rekha P
Rendon A
Renieri A
Renieri A
Renieri A
Rescenko R
Reschreiter H
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Reverter E
Reyes A
Reynolds J
Reynolds T
Reynolds W
Rezk N
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Rice P
Richards JB
Richards JB
Richards JB
Richards O
Richardson N
Richardson N
Riches J
Riches J
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Richmond A
Ridley PM
Riffle S
Rikunenko R
Rime M
Rimoldi V
Ringmets I
Ripamonti D
Ripke S
Rishton C
Risnes K
Ritchie MD
Ritzema J
Riva A
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Rivas M
Riveiro-Barciela M
Rivolta C
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Roberts B
Roberts D
Roberts G
Roberts M
Roberts S
Robertson DL
Robinson M
Robinson P
Rochat-Stettler L
Roche L
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Rodden N
Rodrigues PM
Rodriguez-Frias F
Rodriguez-Gandia M
Roe N
Rogers N
Rogers P
Rogerson K
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Rojo Rello S
Rojo R
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Romani D
Romero-Gomez M
Rooney K
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Rose A
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Rosenberger C
Rosenstiel P
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Rowan K
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Roy A
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Rubinacci S
Ruddy J
Rudkin JK
Ruehlemann MC
Ruiz A
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Russell CD
Russell CD
Russo R
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Rybniker J
Rybniker J
Ryu S
Saad C
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Sabrina R
Sado R
Safa N
Sagara H
Sageshima H
Saha R
Saha R
Saha S
Sahoo M
Sainsbury H
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Saito F
Saito H
Sakagami S
Salberg A
Salciute E
Saleem M
Salerni L
Sales D
Salib I
Salmi S
Salmon K
Salpietro V
Saluja T
Salutous D
Saluzzio RP
Samakomva T
Sampson J
Sanarico M
Sanchez J
Sancho C
Sancho-Shimizu V
Sander LE
Sanderson A
Sandhu R
Sandoval E
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Sands CJ
Sangombe M
Sanguinetti M
Sankaran VG
Sano F
Santoro L
Sarathy V
Sargeant J
Sarma G
Sarzi-Braga S
Sasaki J
Sassa C
Sathe S
Sato T
Sato Y
Satterstrom FK
Saunderson A
Saunderson P
Sauvage A-S
Savage J
Saviciute E
Savill H
Scaggiante F
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Scala M
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Scanlon J
Scarpini E
Schadt EE
Schaefer B
Schaefer M
Scherewode J
Schiaroli E
Schinkel M
Schneider J
Scholefield B
Schommers P
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Schreiber S
Schroeder J
Schroth GP
Schulte EC
Schulte EC
Schulte EC
Schultz MJ
Schulzky M
Schumacher N
Schurmann C
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Schurr E
Schuurman A
Schwartzentruber J
Scolletta S
Scott JT
Scott RH
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Scott T
Scott Z
Scott-Brown J
Scotton PG
Scriven J
Scriven J
Scriven J
Scudeller L
Scudieri P
Sealfon SC
Sealock JM
Seaman R
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Sebra RP
Sedaghati-Khayat B
Seed C
Segala FV
Segala FV
Seilmaier MJ
Sekikawa Y
Sell C
Sellick K
Selvanayagam S
Semple G
Semple MG
Semple MG
Senaratne D
Sengupta S
Seo K
Seok W
SeroCOVID
Serrano-Ruiz A
Shah A
Shah N
Shang N
Shankar-Hari M
Shankar-Hari M
Shankar-Hari M
Shanmuga P
Shanmugasundaram P
Sharma A
Shastri AJ
Shaw CA
Shaw D
Shaw DM
Shaw L
Shaw R
Shaw V
Shaw VE
Shawcross A
Shears RK
Shelley B
Shelton JF
Shelton S
Shen X
Shepardson S
Shepherd A
Shi H
Shibata Y
Shibusawa T
Shiel J
Shih B
Shimada H
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Shimizu T
Shin E
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Shiomi T
Shirai Y
Shiroyama T
Shokkar R
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Shuey MM
Shuker K
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Sicat C
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Sipeky C
Sivanadhan I
Sizer J
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Slater V
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Sloofman L
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Smedley C
Smit M
Smith AV
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Smith O
Smith R
Smith T
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Smits G
Smoller JW
Smuts S
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Solomon T
Solomonson M
Solomonson M
Solomonson M
Sonehara K
Song H
Song K-H
Sonobe K
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Sowter J
Spagnesi M
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Spencer CA
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Spencer S
Spertilli C
Spinner CD
Spittle N
Spivey M
Springle P
Squeo GM
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Stetsenko I
Stevenson L
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Stilma W
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Sugiura H
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Sutherland I
Sutherland S-B
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Takeda Y
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Tanigawa Y
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Tanino Y
Taniyama D
Tanudjaja F
Tariq A
Task HGC
Tateishi T
Tateno H
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Tavecchia L
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Team AC
Team GHR
Tebbutt J
Tedder RS
Teles A
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Tenesa A
Tentorio P
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Terron Arcos V
Tetla D
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Thomas B
Thomas E
Thomas H
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Thompson AAR
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Thompson C
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Thompson R
Thompson RC
Thomson EC
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Thorsteinsdottir U
Thrasyvoulou L
Thrush J
Thwaites RS
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Tilney E
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Tissink E
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Tivenan H
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Todd A
Togashi Y
Tohda S
Tokunaga K
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Tomas AL
Tommasi A
Tomono K
Tonby K
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Tran F
Trankiem A
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Tranter H
Trembath RC
Trembath RC
Tridente A
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Trim F
Trivedi B
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Trochu E
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Trotta T
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Trumper E
Tsao P
Tschopp J
Tselios C
Tsinaslanidis G
Tsonas A
Tsuchida T
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Tucci A
Tuck M
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Tully R
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Turki S
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Turner-Bone I
Turney S
Turtle LCW
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Tyler A
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Uddin MJ
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Ueda S
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Umeda A
Underwood SJ
Urrechaga E
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Utrilla A
Utsugi M
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Vadgama N
Vadla MS
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Valentine J
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Valsecchi MG
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Van Singer M
van Tonder L
van Uffelen KWJ
van Vugt M
Vandernoot I
Varghese M
Vari MS
Varnai R
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Vedage D
Veelo D
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Veerapen K
Veerapen K
Vehreschild MJGT
Velho M
Venkatesh H
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Verdugo RA
Vergori A
Verlander M
Verma A
Verma SS
Vertue M
Vertue M
Verula J
Verzuri A
Viala B
Vigurs C
Vincent R
Vincent-Smith L
Vincenti A
Viollet RM
Visuvanathan S
Vitart V
Vizcaychipi MP
Vlaar APJ
Vochin A
Voide C
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Vollenweider P
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Von Frenckell C
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Vonk JM
Voza A
Vulesevic B
Vuylsteke A
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Wacker EM
Wackett T
Wadams B
Waddington N
Waddy S
Wagstaff V
Waite AAC
Wakabayashi A
Wakahara K
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Walton O
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Wang Q
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Watson E
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Weiss ST
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Welters ID
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Woodyatt W
Woolley AE
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Wyllie DH
Wynter I
Xavier K
Xue X
Yadav A
Yagi K
Yamada M
Yamada Y
Yamagata K
Yamasaki M
Yang G
Yang J
Yang Z
Yaspan B
Yasui Y
Yates B
Yates B
Yatomi M
Ye C
Yengo L
Yermakovich D
Yi X
Yonekawa A
Yoon H
Yoon KJ
Yoshida K
Yoshida S
Yoshida S
Yoshida T
Yoshihara T
Yoshiya K
Yoshiyama T
Youlton N
Younes SE
Young P
Yun N
Zak A
Zaki A
Zambon M
Zamikula J
Zanella A
Zanella I
Zanelli G
Zara F
Zara F
Zarate R
Zarate R
Zborowski AC
Zeberg H
Zechner M
Zechner M
Zguro K
Zhai R
Zhang JE
Zhang M
Zhao JH
Zhen J
Zheng C
Zheng T
Zhou W
Zhou W
Zhu W
Zitter L
Zlatopolsky M
Zoller H
Zollner S
Zongo O
zu Bentrup FM
Zucchi P
Zwinderman AHK
Zyndorf M
Publication venue
Publication date: 01/01/2021
Field of study

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3,4,5,6,7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease