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Your search keyword '"Kwiatkowski, Dominic P [0000-0002-5023-0176]"' showing total 2 results
Start Over Author "Kwiatkowski, Dominic P [0000-0002-5023-0176]" Topic 0302 clinical medicine
2 results on '"Kwiatkowski, Dominic P [0000-0002-5023-0176]"'

1. Assessing transmissibility of SARS-CoV-2 lineage B.1.1.7 in England

Author

Daniel Mair, Adrian Signell, Daniel Laydon, Nadua Bayzid, Clare M McCann, Flavia Flaviani, Thomas Connor, Samir Bhatt, Catherine Moore, Dr Benjamin Lindsey, Malte Pinckert, Jane Masoli, Rachel Blacow, Jacqui Prieto, Ian Harrison, Scott Thurston, Lance Turtle, Thushan De Silva, Gregory Young, Natalie Groves, Andrew Nelson, Angie Lackenby, Lily Geidelberg, Mili Estee Torok, Brendan Payne, Katy Gaythorpe, Sonia Goncalves, Ewan Harrison, Andrew Rambaut, Angela Beckett, David Partridge, Swapnil Mishra, Dimitris Grammatopoulos, Judith Breuer, Jenna Nichols, Erik Volz, Sharon Glaysher, Harry David Wilson, Jack Lee, Marta Gallis, Christophe Fraser, Susan Hopkins, Patrick McClure, Derrick Crook, Juan Ledesma, Theocharis Tsoleridis, Natasha Palmalux, Matthew Dorman, Helen Lowe, Kordo Saeed, Oliver Ratmann, Darren Smith, Gilberto Betancor Quintana, Alan McNally, Matthew Bashton, Steven Rudder, Dennis Wang, Joseph Chappell, Elias Allara, Volz, Erik [0000-0001-6268-8937], Mishra, Swapnil [0000-0002-8759-5902], Geidelberg, Lily [0000-0002-8057-1844], Laydon, Daniel J [0000-0003-4270-3321], Jackson, Ben [0000-0002-9981-0649], Gaythorpe, Katy [0000-0003-3734-9081], Kwiatkowski, Dominic P [0000-0002-5023-0176], Flaxman, Seth [0000-0002-2477-4217], Gandy, Axel [0000-0002-6777-0451], Rambaut, Andrew [0000-0003-4337-3707], Ferguson, Neil M [0000-0002-1154-8093], Apollo - University of Cambridge Repository, Medical Research Council, Bill & Melinda Gates Foundation, and Medical Research Council (MRC)

Subjects
The COVID-19 Genomics UK (COG-UK) consortium, Adult, 0301 basic medicine, Time Factors, Adolescent, General Science & Technology, Lineage (evolution), Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Basic Reproduction Number, Population genetics, Genome, Viral, Biology, law.invention, Evolution, Molecular, Young Adult, 03 medical and health sciences, Age Distribution, 0302 clinical medicine, law, Phylogenetics, Humans, 030212 general & internal medicine, Child, Phylogeny, Aged, Aged, 80 and over, COVID-19 Genomics UK (COG-UK) consortium, Science & Technology, Multidisciplinary, Generation time, SARS-CoV-2, Infant, Newborn, COVID-19, Infant, Middle Aged, Transmissibility (vibration), 3. Good health, Multidisciplinary Sciences, 030104 developmental biology, Transmission (mechanics), England, Evolutionary biology, Child, Preschool, Spike Glycoprotein, Coronavirus, Science & Technology - Other Topics, Basic reproduction number
Abstract

The SARS-CoV-2 lineage B.1.1.7, designated variant of concern (VOC) 202012/01 by Public Health England1, was first identified in the UK in late summer to early autumn 20202. Whole-genome SARS-CoV-2 sequence data collected from community-based diagnostic testing for COVID-19 show an extremely rapid expansion of the B.1.1.7 lineage during autumn 2020, suggesting that it has a selective advantage. Here we show that changes in VOC frequency inferred from genetic data correspond closely to changes inferred by S gene target failures (SGTF) in community-based diagnostic PCR testing. Analysis of trends in SGTF and non-SGTF case numbers in local areas across England shows that B.1.1.7 has higher transmissibility than non-VOC lineages, even if it has a different latent period or generation time. The SGTF data indicate a transient shift in the age composition of reported cases, with cases of B.1.1.7 including a larger share of under 20-year-olds than non-VOC cases. We estimated time-varying reproduction numbers for B.1.1.7 and co-circulating lineages using SGTF and genomic data. The best-supported models did not indicate a substantial difference in VOC transmissibility among different age groups, but all analyses agreed that B.1.1.7 has a substantial transmission advantage over other lineages, with a 50% to 100% higher reproduction number.

Published
2021

2. The ferroportin Q248H mutation protects from anemia, but not malaria or bacteremia

Author

Deepti Gurdasani, James J. Gilchrist, Emily L. Webb, Sodiomon B. Sirima, Thomas N. Williams, Cristina Pomilla, J. Anthony G. Scott, Alison M. Elliott, Dominic P. Kwiatkowski, Anna Rautanen, Swaib A. Lule, Wandia Kimita, Fatou Joof, Reagan M. Mogire, Francis M. Ndungu, Alexander J. Mentzer, Amidou Diarra, Shabir A. Madhi, Philip Bejon, Neema Mturi, Sarah H. Atkinson, Tommy Carstensen, Morgan M. Goheen, Carla Cerami, Adrian V. S. Hill, Alireza Morovat, Kirk A. Rockett, Manjinder S. Sandhu, Andrew M. Prentice, Clare L. Cutland, John Muthii Muriuki, Gavin Band, Muriuki, John Muthii [0000-0003-4369-9547], Mentzer, Alexander J [0000-0002-4502-2209], Band, Gavin [0000-0002-1710-9024], Gilchrist, James J [0000-0003-2045-6788], Carstensen, Tommy [0000-0002-3672-9931], Goheen, Morgan M [0000-0003-2297-3295], Kimita, Wandia [0000-0002-3099-7134], Mogire, Reagan [0000-0001-6454-1613], Cutland, Clare L [0000-0001-8250-8307], Pomilla, Cristina [0000-0002-2581-8365], Gurdasani, Deepti [0000-0001-9996-6929], Rockett, Kirk [0000-0002-6369-9299], Mturi, Neema [0000-0002-6585-2074], Ndungu, Francis M [0000-0002-8977-0030], Sirima, Sodiomon B [0000-0002-0972-4211], Morovat, Alireza [0000-0002-5832-7992], Prentice, Andrew M [0000-0001-5389-451X], Webb, Emily L [0000-0002-4019-7456], Elliott, Alison M [0000-0003-2818-9549], Hill, Adrian VS [0000-0003-0900-9629], Kwiatkowski, Dominic P [0000-0002-5023-0176], Cerami, Carla [0000-0002-7634-0955], Atkinson, Sarah H [0000-0002-8360-4402], Apollo - University of Cambridge Repository, and Wellcome Trust

Subjects
Hemolytic anemia, Male, Erythrocytes, Anemia, Iron, Ferroportin, Mutation, Missense, Bacteremia, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, hemic and lymphatic diseases, parasitic diseases, Medicine, Humans, Health and Medicine, Cation Transport Proteins, Research Articles, 030304 developmental biology, 0303 health sciences, Mutation, Multidisciplinary, biology, business.industry, Infant, Newborn, SciAdv r-articles, Infant, Iron deficiency, Iron Deficiencies, medicine.disease, Hemolysis, 3. Good health, Malaria, Glutamine, Amino Acid Substitution, 030220 oncology & carcinogenesis, Immunology, biology.protein, Female, business, Research Article
Abstract

The FPN Q248H mutation protects children from anemia, hemolysis, and iron deficiency, but not malaria or bacterial infection., Iron acquisition is critical for life. Ferroportin (FPN) exports iron from mature erythrocytes, and deletion of the Fpn gene results in hemolytic anemia and increased fatality in malaria-infected mice. The FPN Q248H mutation (glutamine to histidine at position 248) renders FPN partially resistant to hepcidin-induced degradation and was associated with protection from malaria in human studies of limited size. Using data from cohorts including over 18,000 African children, we show that the Q248H mutation is associated with modest protection against anemia, hemolysis, and iron deficiency, but we found little evidence of protection against severe malaria or bacteremia. We additionally observed no excess Plasmodium growth in Q248H erythrocytes ex vivo, nor evidence of selection driven by malaria exposure, suggesting that the Q248H mutation does not protect from malaria and is unlikely to deprive malaria parasites of iron essential for their growth.

Published
2019

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