Chronic obstructive pulmonary disease (COPD) is the most common chronic respiratory condition in adults. The Global Initiative for Obstructive Lung Disease (GOLD), a collaboration between the World Health Organization and the National Heart Lung and Blood Institute, defines COPD as 'a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious inhaled particles or gases' [
62]. The main etiological agents linked with COPD are cigarette smoking and biomass exposure and the inflammatory response consists of neutrophils, macrophages and CD8+ T cells and, therefore, differs from the allergic inflammation seen in asthma. Pulmonary inflammation is further amplified by oxidative stress and excess proteases released by inflammatory cells recruited to the lung. As in asthma, acute exacerbations are a common occurrence in COPD and become more frequent as the disease progresses [
63]. Exacerbations are a major cause of morbidity, mortality and healthcare costs and accelerate decline in lung function [
64] and quality of life [
65] in COPD patients. Historically, bacterial infections have been considered the predominant infectious etiology, however epidemiological data showing a greater frequency of exacerbations in the winter months [
66] and frequent coryzal symptoms preceding exacerbations suggest a causal role for viruses [
67]. Older studies using cell culture and serologic diagnostic tests detected viral infection in only approximately 10% to 20% of exacerbations [
68,
69]. However, these diagnostic methods have low sensitivity for virus detection especially for RVs that are the most common cause of upper respiratory tract infections. More recent studies using modern PCR-based techniques have allowed a re-evaluation of the importance of viruses in COPD exacerbations and these studies have shown the presence of viruses in 47% to 56% of exacerbations [
70‐
73]. A recent systematic review evaluated weighted mean prevalence of respiratory viruses detected by PCR in patients with acute exacerbations of COPD. Eight studies were included with an overall prevalence of 34.1%, with picornaviruses including RVs being the most frequently detected pathogen, followed by influenza, parainfluenza, RSV and adenoviruses [
74]. Although these studies have higher detection rates they are likely to have underestimated the role of viral infections in COPD exacerbation as they evaluated patients at the time of presentation to healthcare services which often occurs considerably later than the onset of exacerbation and by which time virus may no longer be detectable.