Biomedical Engineering Reference
In-Depth Information
Figure 4
Graph showing the cumulative percentage of viral and nonviral exacerba-
tions recovering symptomatically with respect to time after onset during 150 COPD
exacerbations (p
ΒΌ
0.006). (From Ref. 8.)
We also found that 19 exacerbations were associated with RSV,
though more patients had RSV detected in the stable state than at exacerba-
tion (8). In none of these samples was the RSV detected by culture or serol-
ogy and the detection disappeared when the sensitivity of the PCR was
reduced suggesting that the colonization with virus was low grade. However,
we found that patients in whom RSV was detected were more likely to have
elevated systemic inflammatory markers. This implies that RSV may be a
cause of chronic infection in COPD and further evaluation of the role of
RSV at COPD exacerbation is required. Viruses apart from RSV were
detected in 16.2% of patients with stable COPD by PCR and rhinoviruses
were the most common virus detected in the stable state as well as exacerba-
tion. Recent work by Retmales et al. (25) shows that latent expression of
adenoviral E1 A protein in alveolar epithelial cells may amplify the
effects of cigarette smoke-induced lung inflammation. Thus, chronic viral
infection may be linked to disease severity in COPD and further work is
required on the relation between viruses detected in the stable state and at
exacerbation.
There is now an increasing evidence from experimental rhinovirus infec-
tions that respiratory viruses can infect the lower airway. (26,27). Seemungal
