Two questions, followed from the first infected cell to long after recovery
We study how influenza A virus, SARS-CoV-2 and other respiratory viruses reprogram the cells they infect, and how those changes shape the course of infection and recovery.
Question one
How does infection rewire RNA processing?
Viral infection generates a rich landscape of alternatively processed and translated RNAs and proteins, and almost all of it is missed when you only look at reference genes and transcripts. We hunt for these infection-specific molecules, work out how they arise, and test how they tip host-virus interactions and the outcome of infection.
What we measure
Long-read RNA sequencing
Isoform and reading frame discovery
RNA modifications such as m6A
Ribosome profiling
Question two
How does infection reshape the epigenome?
A virus can dramatically remodel the chromatin landscape of its host cell, changing how genes are regulated during and after infection. We track down the viral and host factors behind this epigenetic reprogramming, and ask a question we find irresistible: do these changes fade once the infection clears, or do they leave a lasting molecular imprint on tissue recovery and long-term health?
What we measure
Chromatin accessibility (ATAC-seq)
Histone modifications (CUT and RUN)
DNA methylation
Recovery time courses
Non-coding RNA, three kinds we follow
Long non-coding RNA
Guides regulatory machinery to specific places.
microRNA
Tunes how much protein a transcript makes.
Circular RNA
Unusually stable, accumulates during infection.
Nucleus
Cytoskeleton
Infected cell
Hover or tap to label the image. Labels are placeholders.
Where we look
iPSC-derived airway models
Human airway epithelium grown from induced pluripotent stem cells
Adult stem cell airway models
Airway cultures derived from adult basal stem cells
Mouse models
In vivo models of respiratory infection and recovery
From discovery to therapy
The big goal? Uncover the fundamental mechanisms of viral disease, and turn those discoveries into new therapies that target both the virus and the damage it leaves in the host.
Discover
Candidates
Prioritise
Shortlist
Validate
Mechanism
Develop
Intervention
Translate
Clinic
After the virus is cleared
Resolution and recovery
Gene programs return to where they started. The tissue repairs and the molecular record of infection fades.
Persistent dysregulation
Some changes stay. Recovery stalls, inflammation lingers and the tissue keeps a molecular imprint.
Which of the two happens, and why, is the question the lab is built around.
Come explore these questions with us
We are always keen to hear from curious, driven people who want to find out what viruses leave behind in our cells. PhD students, postdocs and visiting scientists: say hello.