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Why the common cold poses an extra threat for people with asthma

13 August 2008

New research has identified ways in which rhinovirus infection (the virus behind the common cold) mimics symptoms typical of an asthma attack in people susceptible to the condition. Findings are published in the Proceedings of the National Academy of Sciences (PNAS) this week.

 

Asthma attacks result in around 1,200 deaths a year and cost the NHS approximately £1.0 billion annually. The common cold is one of the main causes of asthma attacks with 90% of people with asthma saying that colds and flu trigger their symptoms, and around 80% of all asthma attacks being caused by such viruses. Despite this, the mechanisms of rhinovirus infection and its links with asthma symptoms and attacks are poorly understood, and clinical evidence supporting how rhinoviruses can cause these symptoms is weak.

 

Following his exciting work, published earlier this year, devising a mouse model for the common cold to explore its role in triggering allergic inflammation of the airways (like that seen in asthma), Professor Sebastian Johnston, at Imperial College London, has been further investigating how rhinovirus infection can cause a reaction within the human body that is typical of an asthma attack.

 

The research, funded jointly by the Medical Research Council, Asthma UK, the British Lung Foundation, the British Medical Association, the National Institute for Health Research, Imperial College London and the Wellcome Trust, investigated responses to rhinovirus infection in 10 people with asthma and 15 control volunteers without asthma. Subjects were given a standard dose of the virus and their reactions were monitored and recorded.

 

After administering the virus both groups had colds of similar severity, but it was found that the volunteers with asthma had a clear increase in asthma symptoms compared with the control volunteers who developed only minimal symptoms. People with asthma also experienced a reduction in lung function and increased airway sensitivity in response to the infection; however this was not seen in the control volunteers.

 

After further analysis, it became apparent that the reaction seen in people with asthma was related to a deficiency in anti-viral immune responses which normally restrict the replication of a virus within the lung, thereby limiting asthma symptoms. With an impaired response, the virus replicates to higher levels, meaning that airway inflammation, and therefore asthma symptoms, are increased.

Although the number of subjects in the study was small, the results mark a new stage in investigations into the causal relationship between rhinovirus infection and asthma symptoms. The model used by Professor Johnston and his colleagues will now form the basis for testing possible future treatments for the worsening of asthma symptoms and asthma attacks as a result of rhinovirus infection. Similarly, novel approaches based on inhibiting viral replication and encouraging protective immune responses may have important therapeutic potential in the treatment of virus-induced asthma attacks in the future.

 

Sebastian L Johnston, Professor of Respiratory Medicine, says “This study has demonstrated clear differences between the responses of asthmatic and normal subjects to rhinovirus infection both in terms of clinical symptoms and airway function.
 
“These observations provide compelling evidence supporting an important role for rhinovirus induced lower airway inflammation in precipitating asthma exacerbations and they identify new avenues for development of novel approaches to therapy.
 
“The study also showed that the reaction seen in people with asthma was related to the severity of their allergic airway inflammation before they were infected. This important finding emphasises the importance of keeping allergic airway inflammation under control by taking asthma controller medications.”

 

Phone: 0207 670 5139
press.office@headoffice.mrc.ac.uk

 

Rhinovirus induced lower respiratory illness is increased in asthma and related to virus load and Th1/2 cytokine and IL-10 production, SL Johnston et al. is published in PNAS.

 

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