Respiratory Syncytial Virus Persistence in Chronic Obstructive Pulmonary Disease

Abstract

Respiratory syncytial virus (RSV) is predominantly recognized as a pediatric pathogen although sensitive molecular diagnostic techniques have led to its more frequent detection in some adult settings. In some studies RSV has been detected just as frequently in stable chronic obstructive pulmonary disease (COPD) patients as in those suffering disease exacerbations, leading to the suggestion that RSV may persist in COPD. Although some studies have found negligible RSV in stable COPD, others have detected RSV in one-quarter to one-third of stable COPD samples. Possible reasons for this discrepancy are explored within the article. A relationship between RSV detection and increased disease severity, including rate of decline in lung function and systemic/airway inflammation, has been found on both occasions it has been sought. Susceptibility to persistent RSV infection could involve both host and viral factors. Cigarette smoking and COPD are likely to result in impaired antiviral immunity, and RSV is capable of evading immune responses by inducing skewed type 2 T-helper cell responses, antagonizing antiviral cytokines, mimicking chemokines, inhibiting apoptosis, and entering immune-privileged cells such as pulmonary neurons. It can also escape an established immune response through antigenic drift. This article examines current evidence regarding persistence of RSV in COPD and its possible mechanisms. We also discuss various roles for RSV persistence in COPD pathogenesis. Further elucidation of the contribution of persistent RSV to the pathogenesis of COPD requires interventional studies. Persistence of RSV in COPD may have direct relevance to the pathogenesis of childhood diseases such as postbronchiolitic wheeze and asthma.

The Lung Tissue Microbiome in Chronic Obstructive Pulmonary Disease

“…These results support the hypothesis that the innate and adaptive immune response contributes to the pathology in peripheral lung lesions in COPD, but the antigens that drive this response remain to be determined (8)(9)(10)(11)(12)(13). Some have suggested that autoantigens drive the pathogenesis of COPD (14), whereas others propose that the emergence of new strains of foreign microbes (9)(10)(11)(15)(16)(17)(18) initiates a cycle of infection, inflammation, and dysfunctional repair, which drives the progression of COPD (10,15).…”

RSV infection modulates IL-15 production and MICA levels in respiratory epithelial cells

“…Interestingly, chronic obstructive pulmonary disease (COPD) is associated with an exaggerated type 1 immune cell inflammatory infiltrate [7,27]. Chronic RSV infection has been reported in COPD [28] and acute COPD exacerbations are associated with RSV infection [29,30]. BORCHERS and co-workers [18,31] demonstrated that NKG2D ligand expression is induced on pulmonary epithelial cells in response to oxidative stress, and protein levels of cell-associated MICA were significantly increased in COPD patients who smoked.…”

Human Metapneumovirus Establishes Persistent Infection in the Lungs of Mice and Is Reactivated by Glucocorticoid Treatment

“…Given the recent discovery of HMPV (73), it is not surprising that substantially more is known about RSV infection, and it is likely that many features linked to RSV will be similar to HMPV (45). RSV and HMPV genome have been detected in chronic obstructive pulmonary disease patients (24,25,49,61,76,78), a feature suggestive of persistent infection. In the mouse model, RSV has been shown to induce long-term airway disease characterized by chronic airway inflammation and airway hyper-reactivity, where 42 days after RSV infection reverse transcription-PCR (RT-PCR) indicated the presence of viral RNA in the lower respiratory tract, and the presence of genomic RNA persisted for months after infection (52).…”