10 research outputs found
Seroprevalence of hepatitis B and C virus in HIV-1 and HIV-2 infected Gambians
- Author
- Publication venue
- BioMed Central
- Publication date
- 01/01/2010
- Field of study
BACKGROUND: The prevalence of HIV/hepatitis co-infection in sub-Saharan Africa is not well documented, while both HIV and HBV are endemic in this area. OBJECTIVE: The aim of this study is to determine the seroprevalence of HBV and HCV virus in HIV-infected subjects in the Gambia. METHODS: Plasma samples from HIV infected patients (190 individuals with clinically defined AIDS and 382 individuals without AIDS) were tested retrospectively for the presence of HBV sero-markers and for serum HBV DNA, screened for HCV infection by testing for anti-HCV antibody and HCV RNA. RESULTS: HBsAg prevalence in HIV-positive individuals is 12.2%. HIV/HBV co-infected individuals with CD4 count of <200 cells µL⁻¹ have a higher HBV DNA viral load than patients with higher CD4 count (log 4.0 vs. log 2.0 DNA copies/ml, p < 0.05). Males (OR = 1.8, 95% CI: 1.0, 3.2) were more likely to be HBsAg positive than female. HCV seroprevalence was 0.9% in HIV-positive individuals. CONCLUSION: The prevalence of HBsAg carriage in HIV- infected Gambians is similar to that obtained in the general population. However co-infected individuals with reduced CD4 levels, indicative of AIDS had higher prevalence of HBeAg retention and elevated HBV DNA levels compared to non-AIDS patients with higher CD4 count
Evaluation of DNA Methylation Episignatures for Diagnosis and Phenotype Correlations in 42 Mendelian Neurodevelopmental Disorders.
- Author
- Afenjar Alexandra
- Ainsworth Peter J
- Alders Mariëlle
- Andrau Jean-Christophe
- Aref-Eshghi Erfan
- Balci Tugce B
- Barat-Houari Mouna
- Bienvenu Thierry
- Brick Lauren
- Campeau Philippe M
- Chatron Nicolas
- Ciolfi Andrea
- Cormier-Daire Valerie
- de Leeuw Nicole
- Dubourg Christèle
- DuPont Barbara R
- Faivre Laurence
- Fergelot Patricia
- Field Michael
- Francastel Claire
- Friez Michael J
- Gecz Jozef
- Genevieve David
- Heide Solveig
- Hennekam Raoul C
- Henneman Peter
- Héron Delphine
- Kadour Mike
- Keren Boris
- Kerkhof Jennifer
- Kleefstra Tjitske
- Kozenko Mariya
- Lacombe Didier
- Laumonnier Frederic
- Lecoquierre François
- Lee Jennifer A
- Lesca Gaetan
- Levy Michael A
- Lin Hanxin
- Mannens Marcel
- Masters Jennifer
- Mignot Cyril
- Nicolas Gaël
- Pedro Victor P
- Pizzi Simone
- Raynaud Martine
- Rodenhiser David I
- Rondeau Sophie
- Rousseau Justine
- Ruiz-Pallares Nathalie
- Sadikovic Bekim
- Sanlaville Damien
- Saugier-Veber Pascale
- Schwartz Charles E
- Shaw Marie
- Siu Victoria Mok
- Skinner Steven A
- Stevenson Roger E
- Stuart Alan
- Takano Kyoko
- Tartaglia Marco
- Tedder Matt
- Thauvin-Robinet Christel
- Ulveling Damien
- Van-Gils Julien
- Velasco Guillaume
- Vitobello Antonio
- Whalen Sandra
- Publication venue
- Scholarship@Western
- Publication date
- 05/03/2020
- Field of study
Genetic syndromes frequently present with overlapping clinical features and inconclusive or ambiguous genetic findings which can confound accurate diagnosis and clinical management. An expanding number of genetic syndromes have been shown to have unique genomic DNA methylation patterns (called episignatures ). Peripheral blood episignatures can be used for diagnostic testing as well as for the interpretation of ambiguous genetic test results. We present here an approach to episignature mapping in 42 genetic syndromes, which has allowed the identification of 34 robust disease-specific episignatures. We examine emerging patterns of overlap, as well as similarities and hierarchical relationships across these episignatures, to highlight their key features as they are related to genetic heterogeneity, dosage effect, unaffected carrier status, and incomplete penetrance. We demonstrate the necessity of multiclass modeling for accurate genetic variant classification and show how disease classification using a single episignature at a time can sometimes lead to classification errors in closely related episignatures. We demonstrate the utility of this tool in resolving ambiguous clinical cases and identification of previously undiagnosed cases through mass screening of a large cohort of subjects with developmental delays and congenital anomalies. This study more than doubles the number of published syndromes with DNA methylation episignatures and, most significantly, opens new avenues for accurate diagnosis and clinical assessment in individuals affected by these disorders
Treatment of invasive fungal infections in cancer patients—Recommendations of the Infectious Diseases Working Party (AGIHO) of the German Society of Hematology and Oncology (DGHO)
- Author
- A Bernard
- A Böhme
- A Glasmacher
- A Nosari
- A Pascual
- A Safdar
- A Safdar
- AC Leenders
- AC Leenders
- AC Reboli
- AE Brouwer
- AF Viollier
- AH Groll
- AH Groll
- AJ Ullmann
- Andrew J. Ullmann
- Angelika Böhme
- BH Segal
- BJ Kullberg
- BJ Spellberg
- C Cordonnier
- C Lass-Flörl
- C Viscoli
- CB Miller
- Christian Junghanss
- CM Horst Van der
- CO Morrissey
- CP Heussel
- CY Chen
- D Caillot
- D Caillot
- D Caillot
- DA Stevens
- Dieter Buchheidt
- Dietmar Reichert
- DP Kontoyiannis
- DP Kontoyiannis
- DP Kontoyiannis
- DW Denning
- DW Denning
- DW Denning
- E Anaissie
- EJ Anaissie
- ER Kuse
- F Offner
- G Maschmeyer
- G Maschmeyer
- G Mattiuzzi
- Georg Maschmeyer
- Gerda Silling
- H Einsele
- Herrmann Einsele
- HH Wolf
- Holger Hebart
- HS Leu
- I Raad
- I Raad
- II Raad
- J Chandra
- J Maertens
- J Maertens
- J Mora-Duarte
- J-AH Burik Van
- JA Larkin
- JD Sobel
- JE Bennett
- JH Rex
- JH Rex
- JI Ito
- JI Ito
- K Hübel
- K Perruccio
- KA Marr
- KW Garey
- L Ostrosky-Zeichner
- L Ostrosky-Zeichner
- L Ostrosky-Zeichner
- L Pagano
- L Pagano
- L Pagano
- L Pagano
- LM Baddour
- M Ellis
- M Ruhnke
- M Tedder
- M v. Eiff
- MA Kish
- Markus Ruhnke
- Meinolf Karthaus
- MH Nguyen
- MR Roden
- MS Saag
- O Penack
- O Ringden
- OA Cornely
- Olaf Penack
- Oliver A. Cornely
- P Matt
- P Phillips
- P Pitisuttithum
- PG Pappas
- PG Pappas
- PG Pappas
- PH Chandrasekar
- R Hachem
- R Herbrecht
- R Herbrecht
- R Herbrecht
- RD DeShazo
- RN Greenberg
- Ruxandra Enzensberger
- RY Hachem
- RY Hachem
- S Harbarth
- S Mousset
- S Sallah
- S Schwartz
- SJ Lin
- Stefan Reuter
- TH Price
- Thomas Kubin
- Thomas Südhoff
- TJ Smith
- TJ Walsh
- TJ Walsh
- TJ Walsh
- Utz Krug
- VJ Anttila
- W Graninger
- W Mills
- Werner Heinz
- WG Powderly
- William Krüger
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Genomic investigations of unexplained acute hepatitis in children
- Author
- Abdulla Amina
- Aebi Christoph
- Agbeko Rachel
- Aggelos Pefanis
- Agranoff Dan
- Agwuh Ken
- Agyeman Philipp
- Alba-Alejandre Irene
- Ali Ladan
- Alkema Wynand
- Allen Karen
- Alrabiah Dimah K.
- Amatya Puja
- Anderson Glenn
- Anderson Suzanne
- Andrade Catarina
- Andreani Julien
- Anpananthar Amutha
- Ansari Imran
- Antinao Diaz Juan F.
- Arif Tasnim
- Armstrong Diane
- Armstrong Jane A.
- Armstrong Lawrence
- Asgarian Zeinab
- Atkinson Laura
- Avcin Tadej
- Avramoska Tanja
- Baas Bryan
- Bahovec Natalija
- Baillie Kenneth
- Balode Anda
- Bamford Alasdair
- Barendregt A. M.
- Barral-Arca Ruth
- Barzdina Arta
- Barzdina Elza
- Basmaci Romain
- Bath David
- Bauchinger Sebastian
- Baumard Lucas
- Baumgart Hinrich
- Baxter Frances
- Bayzid Nadua
- Beer Sally
- Bell Ashley
- Bell Claire
- Bell Kathryn
- Bellini Arianna
- Bello Xabier
- Bellos Evangelos
- Benesch Martin
- Benesch Martin
- Bennet Joshua
- Berger Christoph
- Bernhard-Stirnemann Sara
- Beudeker Coco R.
- Beveridge Laura
- Bibi Sagida
- Bidlingmaier Christoph
- Biesbroek Giske
- Bijukchhe Sanjeev Man
- Billing Kyle
- Binder Alexander
- Binder Vera
- Birt Mark
- Bogovic Petra
- Bohmova Kristyna
- Bojang Kalifa
- Bont Louis J.
- Borensztajn Dorine M.
- Bories Pauline
- Branch Nicole
- Brengel-Pesce Karen
- Breuer Judith
- Broderick Claire
- Brotherton Helen
- Brown Julianne R.
- Brown Rachel
- Buddle Sarah
- Burling Sara
- Buschbeck Judith
- Cabello Laura
- Calle Irene Rivero
- Calvo-Bado Leo
- Campos Luis
- Candlish Janie
- Capozzi Lisa
- Carnota Sandra
- Caro Ivan
- Carrol Enitan D.
- Carson Gail
- Carter Michael
- Carter Michael J.
- Castellano Sergi
- Castro Maria Barreiro
- Cebey-López Miriam
- Ceesay Samba
- Celma Cristina
- Ceolotto Astrid
- Chan Adora
- Chand Meera
- Channon-Wells Samuel
- Charalambos Gogos
- Chikowore Primrose
- Chiurchiù Sara
- Chukkambotla Srikanth
- Chériaux Laura
- Clark Richard
- Clohisey Sara
- Cocklin Elizabeth
- Cohen Jonathan
- Cohen Laure
- Collings Kalvin
- Collins Emma
- Connon Maggie
- Cooray Samantha
- Cotillon Marie
- Counsell John R.
- Coutts Audrey
- Cresswell Fiona
- Crulley Stephen
- Cunnington Aubrey
- Curras-Tuala María José
- Czap Agata
- D'alessandro Umberto
- D?Souza Giselle
- Dall Anna
- Danekova Nevena
- Danhauser Katharina
- Darboe Saffiatou
- Darnell Sarah
- Daubney Esther
- Davis Francesca
- Davoust Juraté
- Dawson Joy
- de Groc Thibault
- de Groot Ronald
- de Haan L.
- de Jonge Marien I.
- de Silva Thushan
- de Tugny Alice
- de Vries Gabriella
- De Surjo
- De Tisham
- Deep Akash
- Deheragoda Maesha
- Deksne D?rta
- Devine Kirsty
- Dewez Juan Emmanuel
- Dewez Manuel
- Diaba Cynthia
- Dickinson Holly
- Dik W.
- Donelly Lorna
- Donohue Chloe
- Dorward David
- Drysdale Simon B.
- Dudley Julia
- Dunning Jake
- DuRand Ingrid
- Eber Ernst
- Eisen Sarah
- Eleftheriou Irini
- Ellis Donna
- Elorrieta Leire Estramiana
- Emonts Marieke
- Ensom Ruth
- Epalza Cristina
- Estrada-Rivadeneyra Diego
- Evans Benjamin
- Fabian Daniel
- Farmer Sarah
- Farto Cristina Balo
- Faust Saul
- Fawkes Angie
- Ferguson Susie
- Fernández Sonia Serén
- Feuchtinger Tobias
- Fidler Katy
- Fink Colin
- Finlayson Lauren
- Fish Matthew
- Fitchett Elizabeth
- Fletcher Tom
- Floyd Sharon
- Fullerton Duncan
- Galassini Rachel
- Gallagher Eileen
- Gallistl Siegfried
- Gannon Louise
- García Mirian Ben
- Gardiner Emma
- Garg Sanjeev
- Geissler J.
- Georgiou Pantelis
- Gerrits G. P. J. M.
- Giannoni Eric
- Gijón Manuel
- Gilchrist Tammy
- Gissen Paul
- Giuseppe Martina Di
- Gloerich Jolein
- Goetschalckx Ines
- Gonzalez Suam
- González Fernando Álvez
- Gores Gunther
- Gormley Stuart
- Graham Clive
- Grammatikopoulos Tassos
- Gravele Dagne
- Griese Matthias
- Grope Ilze
- Gruppen Mariken
- Guerra-Assunção José Afonso
- Gunson Rory
- Gurung Meeru
- Gutiérrez Lourdes
- Gómez-Carballa Alberto
- Haas Nikolaus
- Habgood-Coote Dominic
- Hadzic Nedim
- Hafezi Katarzyna
- Hagedoorn Nienke N.
- Haidl Harald
- Hamilton Shea
- Hamzah Lisa
- Hanlon Killian S.
- Hanson Anita
- Hardwick Hayley
- Harper Rosemary
- Hartshorn Stuart
- Hatcher James
- Hauer Almuthe
- Heidema J.
- Heightman Melissa
- Heininger Ulrich
- Henderson Paul
- Henriet Stefanie
- Herberg Jethro
- Hernández Irene
- Hibberd Martin
- Hickey Naomy
- Ho Antonia Y. W.
- Hodgson Luke
- Hoffmann Florian
- Hoggart Clive
- Holden Jennifer
- Holden Matt
- Hope Susan
- Hopton Sarah
- Hoschler Katja
- Houlihan Catherine
- Hourmat Sara
- Howman Ruth
- Hude Christa
- Huijnen Martijn
- Hutchinson J. Ciaran
- Hösele Susanne
- Iglesias Marisol Vilas
- Iglesias Pilar Leboráns
- Ijaz Samreen
- Ioanna Stergiou
- Irving Clare
- Isaacs John
- Jackson Heather
- Jacques Thomas S.
- Jansen Machiel H.
- Jarman Heather
- Jennings Aislinn
- Jennings Paul
- Jennings Rebecca
- Johnston Joanne
- Jones Amaryl
- Jongerius Ilse
- Jorgensen Rikke
- Juranek Sabrina
- Kaforou Mysini
- Kahlert Christian
- Kandasamy Rama
- Kapper Andreas
- Kappler Matthias
- Karolina Akinosoglou
- Kaufer Benedikt B.
- Kavanagh James
- Keil Julia
- Keldorfer Markus
- Kelgeri Chayarani
- Kelly Dominic F.
- Kelly Sarah
- Kenny Julia
- Khalid Nosheen
- Khanijau Aakash
- Khoo Say
- Kim Eunjung
- King Sharon
- Kishore Shyla
- Kitanovski Lidija
- Kloosterhuis Lieke
- Kohlfürst Daniela S.
- Kohlmaier Benno
- Kolberg Laura
- Kolnik Mojca
- Koshy George
- Krenn Larissa
- Kuijpers Taco
- Kuijpers Taco
- Lachaume Noémie
- Laivacuma Sniedze
- Laivacuma Sniedze
- Law Andrew
- Le Sébastien
- Lee Jack C. D.
- Leigh Simon
- Leiner Tamas
- Leitch Karen
- Leitner Manuel
- Lenihan Rebecca
- Lennon Alexander
- Lett Lauren
- Leurent Baptiste
- Levin Michael
- Lewis-Burke Nadia
- Liebeschuetz Susan
- Lim Emma
- Limb James
- Lin Naomi
- Linforth Michelle
- Little Jeff
- Liu Ching-Chuan
- Logan Sheena
- Lubinda Tim
- Luca Maia De
- Lurz Eberhard
- Löffler Sabine
- MacFarlane Susan
- MacGillivray Louise
- Machín Fátima
- Mackerness Christine
- Maclean Alan
- Maconochie Ian
- Macpherson Hannah
- Madelane Monta
- Maier Esther
- Malcolm Ivone Lancoma
- Mallet François
- Mandal Sema
- Manzanares Ángela
- Manzano Jesus-Rodriguez
- Maritsi Despoina
- Marjaneh Mahdi Moradi
- Markos Maragos
- Marmarinos Antonios
- Marmarinos Antonis
- Martin Bernal Luz Marina
- Martin Alex
- Martin Darran
- Martin Joanne
- Martin Mike
- Martinón-Torres Federico
- Martinón-Torres Nazareth
- Matovu Elijah
- Matthews Peter
- McAlinden Paul
- McArdle Andrew
- McCafferty Sarah
- McDonald Sam
- McDonald Sarah E.
- McDonnell Anne
- McGenily Laura
- McGill Fiona
- McKay Sarah
- Meiere Anija
- Meierford Anne
- Menikou Stephanie
- Merson Laura
- Michalis Voulgarelis
- Miedema C. J.
- Millar Margaret
- Miller Caroline
- Miller Danielle
- Milligan Barry
- Mills Sarah
- Miners Alec
- Mistry Ravi
- Mita Andrew
- Moll Henriëtte A.
- Mommert Marine
- Mommert-Tripon Marine
- Mondo Diana
- Montgomery Kylie-Ann
- Moore Catherine
- Moots Robert
- Moradi Marjaneh Mahdi
- Morfopoulou Sofia
- Morrice John
- Morrice Kirstie
- Morris Craig
- Moser Nicolas
- Muench Georg
- Murdoch David R.
- Murphy Lee
- Mustafa Sobia
- Márquez Sonia
- Nagelkerke Sietse
- Nahtigal Mirijam
- Nasher Magda
- Natalucci Giancarlo
- Neeleman C.
- Neill Claire
- Neshat Samira
- Newal Karen
- Newall Karen
- Ng Joanne
- Nichols Samuel
- Niederer-Loher Anita
- Niedrist Tobias
- Nijman Ruud
- Nijman Ruud
- Nokalna Ieva
- Nordberg Gudrun
- Norris Lucy
- Noursadeghi Mahdad
- Nyirenda Maggie
- O'Connor Daniel
- O?Reilly Peter
- O?Riordan Sean
- Obihara C. C.
- Obosi Lauren
- Odam Miranda
- Oliver Zoe
- Ong Kim-Thanh
- Oosthoek Wilma
- Oosthuyzen Wilna
- Openshaw Peter J. M.
- Ora Miguel Sadiki
- Osterman Veronika
- Owen Dan
- Pachot Alexandre
- Pajkrt D.
- Pajkrt Dasja
- Palmarini Massimo
- Panagiota Lourida
- Papst Lea
- Pardo-Seco Jacobo
- Patel Harsita
- Pathan Nazima
- Paulus Stéphane
- Paulus Stéphane
- Paulus Stéphane C.
- Pavare Jana
- Paz Ivonne Pena
- Pennisi Ivana
- Persand Salina
- Peters Mark
- Pfleger Andreas
- Pfurtscheller Klaus
- Philipsen Ria
- Pickering Ailsa
- Pierce Benjamin
- Pilch Heidemarie
- Pischedda Sara
- Player Jasmine
- Pokhrel Bhishma
- Pokorn Marko
- Pokorn Marko
- Pollara Gabriele
- Pollard Andrew J.
- Pollock Louisa
- Posfay-Barbe Klara M.
- Powell Natassia
- Powell Oliver
- Price Ashley
- Price David
- Price Nicholas
- Prunk Petra
- Pucuka Zanda
- Pérez Belén Mosquera
- Pölz Lena
- Rajic Glorija
- Rampling Tommy
- Ramsay Maxine
- Rashid Aqeela
- Redondo-Collazo Lorenzo
- Reich Jana
- Reid Ruth
- Reiter Karl
- Relly Christa
- Reschreiter Henrik
- Reynolds Tim
- Rhodes Mathew
- Rial Jose Gómez
- Richmond Vivien
- Riddell Anna
- Riedel Thomas
- Robbins Ceri
- Rodríguez Lidia Piñeiro
- Rodríguez-Tenreiro Carmen
- Roff Amy
- Rojo Pablo
- Romaine Sam
- Romani Lorenza
- Roome Tara
- Rosenheim Joshua
- Rowlands Emily
- Roy Sunando
- Rubick Lucy
- Rudzate Aleksandra
- Rughnani Prita
- Russell Clark D.
- Rusu Alexandra
- Rödl Siegfried
- Sagmeister Manfred G.
- Saidykhan Momodou
- Salas Antonio
- Santilli Giorgia
- Sarr Anna RocaIsatou
- Schlapbach Luregn
- Schlapbach Luregn J.
- Schlüchter Stefanie
- Schmied Patricia
- Schoen Carola
- Scholefield Barnaby J.
- Schonenberg D.
- Schonenberg Dieneke
- Schranz Rachel
- Schroepf Sebastian
- Schweintzger Nina A.
- Schöbi Nina
- Seal Matthew
- Secka Fatou
- Segal Terry
- Selecka Katrina
- Semple Malcolm Gracie
- Shackley Fiona
- Shah Priyen
- Shaji Mariya
- Shankar-Hari
- Shaw Victoria
- Shen Ching-Fen
- Shenton Geoff
- Shepherd Samantha J.
- Shrestha Shrijana
- Siam Ala?a
- Sidorova Aleksandra
- Simagan Teresa
- Simmonds Peter
- Simmons Ruth
- Skrabl-Baumgartner Andrea
- Solomon Tom
- Spencer Collette
- Sperl Matthias
- Sprenkeler Evelien
- Spyridis Nikos
- Srovin Tina Plankar
- Srpcic Anja
- Stampfer Laura
- Steele Michael
- Stevens Jake
- Stevens Molly
- Stocker Martin
- Stoiser Bianca
- Stoldere Diana
- Storey Nathaniel
- Strempfl Martina
- Strenger Volker
- Strijbosch Annelieke M.
- Strle Franc
- Suárez Carlos Durán
- Svile Dace
- Swingler Rachel
- Syggelou Kelly
- Sánchez José María Martinón
- Sée Hélène
- Tait Sarah
- Talts Tiina
- Tambouratzi Maria
- Tan Chantal
- Tappouni Luke J.
- Tauchert Maike K.
- Tavliavini Emma
- Tayler Rachel
- Tedder Richard S.
- Tempel Dennie
- Templeton Kate
- Thalassinos Konstantinos
- Thomas Daisy
- Thomson Emma
- Thomson Evelyn
- Thorson Stephen
- Tibby Shane
- Till Holger
- Tissing Wim J. E.
- Tkhayat Raja Ben
- Torres Montaguth Oscar Enrique
- Tramper-Stranders G. A.
- Trasorras Cristina Serén
- Treloar Owen
- Trobisch Andreas
- Tsolia Maria
- Turtle Lance C. W.
- Tutill Helena
- Urbane Urzula Nora
- Ushiro-Lumb Ines
- Usman Mariama
- Usuf Effua
- Valentine Lucille
- van Aerde Koen
- van de Kuip Martijn
- van den Berg J. M.
- van den Berg Merlijn
- van den Broek Bryan
- van der Flier Michiel
- van der Flier Michiel
- van der Giessen Ilona
- van der Kuip M.
- van der Velden Fabian
- van der Velden Fabian J. S.
- van der Zee Carlijn
- van Furth A. M.
- van Furth Marceline
- van Gool Alain J.
- van Hensbroek Michael Boele
- van Keulen Danielle
- van Leur M.
- van Mierlo G.
- Vastert Sebastiaan J.
- Venturini Cristina
- Vergnault Nathalie
- Verkuil Floris
- Vermont Clementien L.
- Vicente Luisa García
- Vijlbrief Daniel C.
- Villaverde Serena
- Vincek Katarina
- Vito Ortensia
- Voice Marie
- von Both Ulrich
- Vázquez Sara Rey
- Waddington Simon N.
- Wallia Diane
- Wallner Elmar
- Wang Shih-Min
- Ward Bryony
- Ward Catriona
- Watson Conall
- Weber Kathrin
- Wedderburn Catherine
- Wellings Lucy
- Wellman Paul
- Wham Murray
- White Deborah
- White Marie
- Whittaker Elizabeth
- Whittaker Paul
- Whittaker Thomas E.
- Willems Esther
- Williams Charlotte A.
- Williams Rachel
- Wilson Barbara
- Wilson Clare
- Winmill Helen
- Wolfs Tom F. W.
- Womersley Rebecca
- Wood Amanda
- Woodsford Phil
- Wright Victoria
- Wrobel Nicola
- Wyss Verena
- Wösten-van Asperen Roelie M.
- Xagorari Marietta
- Yeung Shunmay
- Zachariasse Joany
- Zaman Syed M. A.
- Zambon Maria
- Zandstra Judith
- Zavadska Dace
- Zennezini Chiozzi Riccardo
- Zenz Werner
- Zimmermann Elisa
- Zurl Christoph
- Zwerenz Manuela
- Publication venue
- Nature Research
- Publication date
- 30/03/2023
- Field of study
Since its first identification in Scotland, over 1,000 cases of unexplained paediatric hepatitis in children have been reported worldwide, including 278 cases in the UK1. Here we report an investigation of 38 cases, 66 age-matched immunocompetent controls and 21 immunocompromised comparator participants, using a combination of genomic, transcriptomic, proteomic and immunohistochemical methods. We detected high levels of adeno-associated virus 2 (AAV2) DNA in the liver, blood, plasma or stool from 27 of 28 cases. We found low levels of adenovirus (HAdV) and human herpesvirus 6B (HHV-6B) in 23 of 31 and 16 of 23, respectively, of the cases tested. By contrast, AAV2 was infrequently detected and at low titre in the blood or the liver from control children with HAdV, even when profoundly immunosuppressed. AAV2, HAdV and HHV-6 phylogeny excluded the emergence of novel strains in cases. Histological analyses of explanted livers showed enrichment for T cells and B lineage cells. Proteomic comparison of liver tissue from cases and healthy controls identified increased expression of HLA class 2, immunoglobulin variable regions and complement proteins. HAdV and AAV2 proteins were not detected in the livers. Instead, we identified AAV2 DNA complexes reflecting both HAdV-mediated and HHV-6B-mediated replication. We hypothesize that high levels of abnormal AAV2 replication products aided by HAdV and, in severe cases, HHV-6B may have triggered immune-mediated hepatic disease in genetically and immunologically predisposed children
Effects of Anacetrapib in Patients with Atherosclerotic Vascular Disease
- Author
- Aaltonen M
- Abdur Rahman M
- Abell T
- Abide W. Jr
- Acheatel R
- Achiri P
- Acon J
- Adams T
- Affinito S
- Agarwal S
- Aggarwal K
- Aggarwal R
- Ahlström P
- Ahmad A
- Ahmed M
- Aillon C
- Airaksinen A
- Ait-sadi R
- Akers J
- Al-jumaily J
- Albers C
- Albert M
- Alberti A
- Alexander T
- Alford C
- Algotsson L
- Allen T
- Allworth M
- Almond E
- Aloisi A
- Alternburg C
- Alton M
- Amin J
- Amundson A
- Andersen K
- Andersen M
- Anderson E
- Anderson G
- Anderson R
- Anderson T
- Andersson H
- Andersson L
- Andreo J
- Andres C
- Andresen D
- Andrews G
- Andrews L
- Andrews R
- Andrioli V
- Angermann Ce
- Annas T
- Ansell V
- Antonio-drabek C
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- Zhou Yingyuan
- Zhu Wangqin
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- Zlatewa R
- Zoghbi J
- Zong C
- Zong D
- Zong X
- Zuchelkowski A
- Zulauf N
- Ågårdh A
- Öner A
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2017
- Field of study
BACKGROUND:
Patients with atherosclerotic vascular disease remain at high risk for cardiovascular events despite effective statin-based treatment of low-density lipoprotein (LDL) cholesterol levels. The inhibition of cholesteryl ester transfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipoprotein (HDL) cholesterol levels. However, trials of other CETP inhibitors have shown neutral or adverse effects on cardiovascular outcomes.
METHODS:
We conducted a randomized, double-blind, placebo-controlled trial involving 30,449 adults with atherosclerotic vascular disease who were receiving intensive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92 mg per deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol per liter). The patients were assigned to receive either 100 mg of anacetrapib once daily (15,225 patients) or matching placebo (15,224 patients). The primary outcome was the first major coronary event, a composite of coronary death, myocardial infarction, or coronary revascularization.
RESULTS:
During the median follow-up period of 4.1 years, the primary outcome occurred in significantly fewer patients in the anacetrapib group than in the placebo group (1640 of 15,225 patients [10.8%] vs. 1803 of 15,224 patients [11.8%]; rate ratio, 0.91; 95% confidence interval, 0.85 to 0.97; P=0.004). The relative difference in risk was similar across multiple prespecified subgroups. At the trial midpoint, the mean level of HDL cholesterol was higher by 43 mg per deciliter (1.12 mmol per liter) in the anacetrapib group than in the placebo group (a relative difference of 104%), and the mean level of non-HDL cholesterol was lower by 17 mg per deciliter (0.44 mmol per liter), a relative difference of -18%. There were no significant between-group differences in the risk of death, cancer, or other serious adverse events.
CONCLUSIONS:
Among patients with atherosclerotic vascular disease who were receiving intensive statin therapy, the use of anacetrapib resulted in a lower incidence of major coronary events than the use of placebo. (Funded by Merck and others; Current Controlled Trials number, ISRCTN48678192 ; ClinicalTrials.gov number, NCT01252953 ; and EudraCT number, 2010-023467-18 .)
Mapping the human genetic architecture of COVID-19
- Author
- Abdelrazik M.
- Abdullah T.
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- Zlatopolsky M.
- Zoller H.
- Zollner S.
- Zongo O.
- Zucchi P.
- Zyndorf M.
- 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
Erratum: Evaluation of DNA Methylation Episignatures for Diagnosis and Phenotype Correlations in 42 Mendelian Neurodevelopmental Disorders (The American Journal of Human Genetics (2020) 106(3) (356–370), (S0002929720300197), (10.1016/j.ajhg.2020.01.019))
- Author
- Afenjar Alexandra
- Ainsworth Peter J.
- Alders Mariëlle
- Andrau Jean-Christophe
- Aref-Eshghi Erfan
- Balci Tugce B.
- Barat-Houari Mouna
- Bienvenu Thierry
- Brick Lauren
- Campeau Philippe M.
- Chatron Nicolas
- Ciolfi Andrea
- Cormier-Daire Valerie
- de Leeuw Nicole
- Dubourg Christéle
- DuPont Barbara R.
- Faivre Laurence
- Fergelot Patricia
- Field Michael
- Francastel Claire
- France Groupe D. I.
- Friez Michael J.
- Gecz Jozef
- Genevieve David
- Heide Solveig
- Hennekam Raoul C.
- Henneman Peter
- Héron Delphine
- Kadour Mike
- Keren Boris
- Kerkhof Jennifer
- Kleefstra Tjitske
- Kozenko Mariya
- Lacombe Didier
- Laumonnier Frederic
- Lecoquierre François
- Lee Jennifer A.
- Lesca Gaetan
- Levy Michael A.
- Lin Hanxin
- Mannens Marcel
- Masters Jennifer
- Mignot Cyril
- Nicolas Gaël
- Pedro Victor P.
- Pizzi Simone
- Raynaud Martine
- Rodenhiser David I.
- Rondeau Sophie
- Rousseau Justine
- Ruiz-Pallares Nathalie
- Sadikovic Bekim
- Sanlaville Damien
- Saugier-Veber Pascale
- Schwartz Charles E.
- Shaw Marie
- Siu Victoria Mok
- Skinner Steven A.
- Stevenson Roger E.
- Stuart Alan
- Takano Kyoko
- Tartaglia Marco
- Tedder Matt
- Thauvin-Robinet Christel
- Ulveling Damien
- van-Gils Julien
- Velasco Guillaume
- Vitobello Antonio
- Whalen Sandra
- Publication venue
- 'Elsevier BV'
- Publication date
- 03/06/2021
- Field of study
(The American Journal of Human Genetics 106, 356–370; March 5, 2020) In the version of this paper originally published, the underlying cause for Hunter McAlpine syndrome was incorrectly described in Table 1. The relevant description has been changed to read “Chr5q35-qter duplication involving NSD1” in the updated Table 1 reflected here. The authors apologize for this error
Recommended from our members
GWAS and meta-analysis identifies 49 genetic variants underlying critical COVID-19
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- Publication venue
- Springer Nature
- Publication date
- 17/05/2023
- Field of study
Data availability: Downloadable summary data are available through the GenOMICC data site (https://genomicc.org/data). Summary statistics are available, but without the 23andMe summary statistics, except for the 10,000 most significant hits, for which full summary statistics are available. The full GWAS summary statistics for the 23andMe discovery dataset will be made available through 23andMe to qualified researchers under an agreement with 23andMe that protects the privacy of the 23andMe participants. For further information and to apply for access to the data, see the 23andMe website (https://research.23andMe.com/dataset-access/). All individual-level genotype and whole-genome sequencing data (for both academic and commercial uses) can be accessed through the UKRI/HDR UK Outbreak Data Analysis Platform (https://odap.ac.uk). A restricted dataset for a subset of GenOMICC participants is also available through the Genomics England data service. Monocyte RNA-seq data are available under the title ‘Monocyte gene expression data’ within the Oxford University Research Archives (https://doi.org/10.5287/ora-ko7q2nq66). Sequencing data will be made freely available to organizations and researchers to conduct research in accordance with the UK Policy Framework for Health and Social Care Research through a data access agreement. Sequencing data have been deposited at the European Genome–Phenome Archive (EGA), which is hosted by the EBI and the CRG, under accession number EGAS00001007111.Extended data figures and tables are available online at https://www.nature.com/articles/s41586-023-06034-3#Sec21 .Supplementary information is available online at https://www.nature.com/articles/s41586-023-06034-3#Sec22 .Code availability:
Code to calculate the imputation of P values on the basis of SNPs in linkage disequilibrium is available at GitHub (https://github.com/baillielab/GenOMICC_GWAS).Acknowledgements: We thank the members of the Banco Nacional de ADN and the GRA@CE cohort group; and the research participants and employees of 23andMe for making this work possible. A full list of contributors who have provided data that were collated in the HGI project, including previous iterations, is available online (https://www.covid19hg.org/acknowledgements).Change history: 11 July 2023: A Correction to this paper has been published at: https://doi.org/10.1038/s41586-023-06383-z. -- In the version of this article initially published, the name of Ana Margarita Baldión-Elorza, of the SCOURGE Consortium, appeared incorrectly (as Ana María Baldion) and has now been amended in the HTML and PDF versions of the article.Copyright © The Author(s) 2023, Critical illness in COVID-19 is an extreme and clinically homogeneous disease phenotype that we have previously shown1 to be highly efficient for discovery of genetic associations2. Despite the advanced stage of illness at presentation, we have shown that host genetics in patients who are critically ill with COVID-19 can identify immunomodulatory therapies with strong beneficial effects in this group3. Here we analyse 24,202 cases of COVID-19 with critical illness comprising a combination of microarray genotype and whole-genome sequencing data from cases of critical illness in the international GenOMICC (11,440 cases) study, combined with other studies recruiting hospitalized patients with a strong focus on severe and critical disease: ISARIC4C (676 cases) and the SCOURGE consortium (5,934 cases). To put these results in the context of existing work, we conduct a meta-analysis of the new GenOMICC genome-wide association study (GWAS) results with previously published data. We find 49 genome-wide significant associations, of which 16 have not been reported previously. To investigate the therapeutic implications of these findings, we infer the structural consequences of protein-coding variants, and combine our GWAS results with gene expression data using a monocyte transcriptome-wide association study (TWAS) model, as well as gene and protein expression using Mendelian randomization. We identify potentially druggable targets in multiple systems, including inflammatory signalling (JAK1), monocyte–macrophage activation and endothelial permeability (PDE4A), immunometabolism (SLC2A5 and AK5), and host factors required for viral entry and replication (TMPRSS2 and RAB2A).GenOMICC was funded by Sepsis Research (the Fiona Elizabeth Agnew Trust), the Intensive Care Society, a Wellcome Trust Senior Research Fellowship (to J.K.B., 223164/Z/21/Z), the Department of Health and Social Care (DHSC), Illumina, LifeArc, the Medical Research Council, UKRI, a BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070 and BBS/E/D/30002275) and UKRI grants MC_PC_20004, MC_PC_19025, MC_PC_1905 and MRNO2995X/1. A.D.B. acknowledges funding from the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z), the Edinburgh Clinical Academic Track (ECAT) programme. This research is supported in part by the Data and Connectivity National Core Study, led by Health Data Research UK in partnership with the Office for National Statistics and funded by UK Research and Innovation (grant MC_PC_20029). Laboratory work was funded by a Wellcome Intermediate Clinical Fellowship to B.F. (201488/Z/16/Z). We acknowledge the staff at NHS Digital, Public Health England and the Intensive Care National Audit and Research Centre who provided clinical data on the participants; and the National Institute for Healthcare Research Clinical Research Network (NIHR CRN) and the Chief Scientist’s Office (Scotland), who facilitate recruitment into research studies in NHS hospitals, and to the global ISARIC and InFACT consortia. GenOMICC genotype controls were obtained using UK Biobank Resource under project 788 funded by Roslin Institute Strategic Programme Grants from the BBSRC (BBS/E/D/10002070 and BBS/E/D/30002275) and Health Data Research UK (HDR-9004 and HDR-9003). UK Biobank data were used in the GSMR analyses presented here under project 66982. The UK Biobank was established by the Wellcome Trust medical charity, Medical Research Council, Department of Health, Scottish Government and the Northwest Regional Development Agency. It has also had funding from the Welsh Assembly Government, British Heart Foundation and Diabetes UK. The work of L.K. was supported by an RCUK Innovation Fellowship from the National Productivity Investment Fund (MR/R026408/1). J.Y. is supported by the Westlake Education Foundation. SCOURGE is funded by the Instituto de Salud Carlos III (COV20_00622 to A.C., PI20/00876 to C.F.), European Union (ERDF) ‘A way of making Europe’, Fundación Amancio Ortega, Banco de Santander (to A.C.), Cabildo Insular de Tenerife (CGIEU0000219140 ‘Apuestas científicas del ITER para colaborar en la lucha contra la COVID-19’ to C.F.) and Fundación Canaria Instituto de Investigación Sanitaria de Canarias (PIFIISC20/57 to C.F.). We also acknowledge the contribution of the Centro National de Genotipado (CEGEN) and Centro de Supercomputación de Galicia (CESGA) for funding this project by providing supercomputing infrastructures. A.D.L. is a recipient of fellowships from the National Council for Scientific and Technological Development (CNPq)-Brazil (309173/2019-1 and 201527/2020-0)
Mapping the human genetic architecture of COVID-19
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- 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