High levels of Epstein-Barr virus in COPD.

Latent viral infection has been implicated in the pathophysiology of chronic obstructive pulmonary disease (COPD). Epstein-Barr virus (EBV) is known to be important in pulmonary fibrosis. The current authors hypothesised that EBV is associated with the pathogenesis of COPD. Sputum samples were collected from patients both during exacerbations of COPD and when stable. A control group of smokers who did not have airways obstruction also had their sputum examined. The presence of EBV DNA was established and quantified using a real-time nucleic acid amplification assay. A total of 136 patients with COPD were recruited during an acute exacerbation and a total of 68 when stable. EBV was detected in 65 (48%) exacerbation cases and 31 (46%) stable patients. In the comparison group of 16 nonobstructed smokers, EBV was demonstrated in only one (6%) case. Risk of COPD in patients with EBV and who are smokers confers an odds ratio of 12.6. Epstein-Barr virus DNA is more frequently identified in the respiratory tract of chronic obstructive pulmonary disease patients in comparison with unaffected smokers. It is present both during exacerbation and when stable, suggesting that infection is persistent. Smokers who do not develop chronic obstructive pulmonary disease rarely have Epstein-Barr virus in their sputum. This finding may be of importance in the pathogenesis of chronic obstructive pulmonary disease.

Childhood respiratory infections and hospital admissions for COPD.

BACKGROUND: Chronic Obstructive Pulmonary Disease (COPD) exacerbations are associated with viral infections. We wished to determine if respiratory viral infection of children in the community was associated with hospital admissions of patients with exacerbations of COPD. METHODS: We collected data over a 45-month period from the Northern Ireland Regional Virus Laboratory and from a general hospital in the same locality. We studied the relationship between upper respiratory infections in children and COPD admissions. We also examined the role of school holidays. RESULTS: Correlations were seen between the frequency of all viral infections in children and the number of adult COPD hospitalizations (P<0.005). Subgroup analysis showed distinct relationships with epidemics of; influenza A (P<0.001), influenza B (P<0.05), adenovirus (P=0.05), respiratory syncytial virus (P<0.005) and hospital admissions of patients with COPD. There were significantly fewer COPD admissions in the week after the start of a school holiday period (P<0.05). CONCLUSIONS: When children are hospitalized with viral respiratory infection there is an associated rise in adult COPD admissions. This suggests exacerbations of COPD are associated with epidemics of respiratory viruses. When children are on school holidays there is a reduction in COPD admissions in the community. This provides further support for respiratory viruses in the pathogenesis of COPD exacerbations.

Cystic fibrosis genotype and bacterial infection: a possible connection.

Patients with cystic fibrosis (CF) have repeated bacterial infection of the airways, which can lead to chronic infection. There is evidence that disease severity is determined by the genetic mutations present. This study aims to establish if CF genotype is related to the frequency and types of airway bacterial infection. Adult patients attending the regional CF unit are followed for two years and assigned to one of three groups depending on whether they are chronically infected with Burkholderia cepacia complex (BCC) organisms, Pseudomonas aeruginosa, or neither of these organisms. Genotype analysis is performed on all patients to determine which of the cystic fibrosis transmembrane regulator (CFTR) gene mutations are present. The numbers and types of organism with the CFTR mutations isolated from sputum are identified. Data are available on 59 patients: 15 colonised with BCC, 24 colonised with P. aeruginosa, and 20 not colonised with either organism. Twenty patients were homozygous for deltaF508, 25 were heterozygous, and the deltaF508 mutation was not present in the remaining 14 patients. Patients homozygous or heterozygous for the deltaF508 mutation had an increased likelihood of colonisation with BCC or P. aeruginosa, an increased number of positive sputum cultures and a higher frequency of multiple infecting organisms. Cystic fibrosis mutational analysis identified seven patients who had the R117H mutation. These patients were less likely to be colonised with BCC or P. aeruginosa. In conclusion, patients homozygous or heterozygous for the deltaF508 deletion are more likely to suffer airway colonisation with BCC or P. aeruginosa, with increased numbers of positive sputum cultures and infecting organisms. Those with the R117H mutation are less likely to be colonised by Gram-negative organisms.