William Cookson

Professor William Cookson serves as Professor of Genomic Medicine at Imperial College London's National Heart & Lung Institute within the Faculty of Medicine. He heads the Asmarley Centre for Genomic Medicine and maintains affiliations with the CRUK Convergence Science Centre, Cancer Technology Network, Fungal Science Network, Genomic and Environmental Medicine, Immuno-Pathology Network, and Microbiome Network.

His educational background includes respiratory physician training and a D.Phil. in Human Genetics from the University of Oxford (1994). Previously, he held a Professorship in Human Genetics at Oxford (1998-2004).

Cookson's research centers on asthma genetics and airway microbiome interactions, identifying critical genes (ORMDL3, IL33, TSLP, IL18R1) now targeted for novel therapies. His team pioneered airway microbiome characterization through DNA sequencing, revealing dysbiosis in asthma/COPD and discovering over 50 new bacterial species. Current work focuses on translating findings into antivirals, inhaled antimicrobials, and vaccines following pandemic-era observations of reduced respiratory disease.

Recent publications demonstrate consistent innovation across genomics, immunology, and microbiology, with landmark studies spanning asthma genetics (2003-2015) and microbiome science (2010-present). His work increasingly integrates environmental interaction models and therapeutic development.

His accolades include:

• Joint Wellcome Senior Investigator Award (2011)
• NIHR Senior Investigator status (2013)
• Fellowship of the Academy of Medical Sciences
• Membership in the European Academy of Arts and Sciences

Leading a research group with Professor Miriam Moffatt for over 30 years, Cookson secured major funding including the Wellcome award and GABRIEL consortium coordination. His work drives public health strategies like school-based viral protection for asthmatic children. The Asmarley Centre for Genomic Medicine serves as his primary research hub, leveraging genomic sequencing and culture-independent methods across pulmonary fibrosis, cystic fibrosis, and bronchiectasis studies.