MRVCOPD: Using Multiomics to define mechanisms of RhinoVirus-induced Chronic Obstructive Pulmonary Disease exacerbations to develop novel therapies and therapeutic targets
Recipient organisationNIHR Wellcome Trust Imperial Clinical Research Facility
NIHR supportRecorded as supported by this research centre
PeriodMar 2025 — Apr 2027
In plain English
AI plain-English summary
A common cold virus triggers severe lung flare-ups in 95% of people with COPD, and researchers are now deliberately infecting volunteers to study exactly how this happens. COPD is the fourth leading cause of death globally, killing 3.5 million people in 2021. The sudden symptom flare-ups called acute exacerbations are driven largely by viral infections, yet the biological mechanisms inside the lungs during these events remain poorly understood. Studying natural exacerbations is unreliable and repeated lung sampling can be dangerous, so the team developed a controlled human rhinovirus challenge model. By comparing COPD patients with healthy smokers and non-smokers, they will use multiomics techniques—analysing genes, proteins, and metabolites together—to map the molecular chain of events that turns a cold into a life-threatening exacerbation. If this succeeds, the data will reveal specific biological targets for new drugs that could reduce the frequency and severity of COPD exacerbations. The findings will be made publicly available and integrated with other databases, maximising the scientific return from each participant’s contribution. This is translational research with a direct path to therapy development.
View original technical description
We aim to understand the biological mechanisms that underlie exacerbations of Chronic Obstructive Pulmonary Disease (COPD) to drive the discovery of new treatments. COPD is the 4th leading cause of death worldwide, causing 3.5 million deaths in 2021. Acute exacerbations of COPD (AECOPD) involve sudden flare-ups of symptoms, commonly triggered by viral infections, and are the major cause of COPD morbidity, mortality and healthcare costs. Developing new treatments for AECOPD requires a better understanding of the processes occurring in the lungs, before and during exacerbations. Naturally-occuring AECOPD are challenging to study in a way that allows reliable measurement of disease mechanisms, and repeated lung sampling can be impractical and potentially dangerous. We therefore developed a human rhinovirus challenge experimental model of AECOPD. This involves infecting participants in our study with a common cold virus called rhinovirus (RV). We have demonstrated that RV causes mildto- moderate exacerbations in 95% of COPD subjects, that we can control confounding factors to take reliable measurements, and that we can safely and easily perform repeated sampling of the lungs and respiratory tract. We will compare people who have COPD with people who do not have COPD, including smokers and non-smokers, to identify the processes important in COPD. We will measure a range of clinical and scientific outcomes, using cutting-edge ‘multiomics’ techniques to understand mechanisms in RV-induced AECOPD to an extent that has not been achieved before. The crucial information that this study generates will be used to identify new treatments to reduce the frequency and severity of AECOPD. Our data will be made publicly available for others to use and analyse, and will be integrated with other databases to maximise the scientific benefit that is gained from our participants' contribution to the project.
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