Human rhinoviruses (RV) are the most common human pathogens, triggering the majority of upper respiratory viral infections (URIs), such as the common cold, and exacerbating asthma and chronic obstructive pulmonary disease.
The impact of these infections is huge: URIs account for approximately 50% of all illnesses and 75% of all illnesses in young children. They result in more than 150 million days of work absence, with an economic cost in lost productivity approaching $25 billion. In addition, over $10 billion in medical bills are racked up by common colds annually in the USA. Over £500 million is spent in the UK every year on over-the-counter medicines for coughs and colds and antibiotics are prescribed in up to 60% of patients with common colds. Asthma exacerbations not only increase the economic impact by several billion, but also represent severe and occasionally fatal conditions.
More than half of all of the above events are directly associated with RV. There is therefore no doubt that preventing RV infection and/or its consequences will have a major impact on human health around the planet.
One of the major challenges in designing an RV vaccine or targeted antiviral drug is the high variability of these viruses, as well as our incomplete knowledge of how viruses’ molecular structure and disease-causing properties change over time. It is possible that RVs exist as molecularly variable populations, capable of escaping therapies, which target specific parts of them. Such a hurdle may be overcome by identifying and targeting key parts of the virus, which are crucial for the virus population survival.
Professor Nikos Papadopoulos has recently moved to The University of Manchester. For more than 15 years he has been investigating the mechanisms of RV infection and RV-induced asthma exacerbations. He is currently leading PreDicta, an EU FP7 funded collaborative project, evaluating the hypothesis that repeated viral infections may reprogram the immune system into a hyper-reactive state, leading to persistence of asthma. Within this project, anti-RV therapies are being explored and a chip capable of measuring the immune response against different RV subtypes is being developed. Professor Papadopoulos is also developing new models to study the interactions of the virus with the immune system, which can be used to compare how effective different antiviral molecules are in treating RV and to study the development of antibodies in response to one or more viral exposures.