Respiratory viruses in exacerbations of chronic obstructive pulmonary disease requiring hospitalisation: a case-control study

Rohde, Gernot; Wiethege, Almut; Borg, Irmgard; Kauth, Marion; Bauer, TT; Gillissen, Adrian; Bufe, Albrecht; Schultze‐Werninghaus, G.

doi:10.1136/thorax.58.1.37

Cited by 487 publications

(465 citation statements)

References 30 publications

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“…Greenberg documented that 27% of exacerbations in 62 prospectively followed patients with COPD were related to a viral etiology (45); picornaviruses, parainfluenza virus, and coronaviruses accounted for the majority of infections in this study. Other investigators have suggested that up to 60% of exacerbations have been associated with viral infections, including picornaviruses, respiratory syncytial virus (RSV), influenza, and human metapneumoviruses (46)(47)(48)(49)(50)(51). One prospective study of hospitalized patients with AE-COPDs found a viral pathogen in more than 48% of episodes (vs. 6.25% in the stable state), with a similar distribution of viral pathogens as previously noted (52).…”

Section: Virusessupporting

confidence: 55%

Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Martínez

2007

Proceedings of the American Thoracic Society

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Acute exacerbations of chronic obstructive pulmonary disease (COPD) are important events in the natural history of this chronic lung disorder. These events can be caused by a large number of infectious and noninfectious agents and are associated with an increased local and systemic inflammatory response. Their frequency and severity have been linked to progressive deterioration in lung function and health status. Infectious pathogens ranging from viral to atypical and typical bacteria have been implicated in the majority of episodes. Most therapeutic regimens to date have emphasized broad, nonspecific approaches to bronchoconstriction and pulmonary inflammation. Increasingly, therapy that targets specific etiologic pathogens has been advocated. These include clinical and laboratory-based methods to identify bacterial infections. Further additional investigation has suggested specific pathogens within this broad class. As specific antiviral therapies become available, better diagnostic approaches to identify specific pathogens will be required. Furthermore, prophylactic therapy for at-risk individuals during high-risk times may become a standard therapeutic approach. As such, the future will likely include aggressive diagnostic algorithms based on the combination of clinical syndromes and rapid laboratory modalities to identify specific causative bacteria or viruses.

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Section: Virusessupporting

confidence: 55%

Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Martínez

2007

Proceedings of the American Thoracic Society

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“…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.…”

Section: Ifn-c Increases Rsv-induced Il-15 Levels But Downregulates Rmentioning

confidence: 99%

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

Zdrenghea¹,

Telcian²,

Laza-Stanca³

et al. 2011

Eur Respir J

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The cytokine interleukin (IL)-15, major histocompatibility complex (MHC) class I molecules and MHC class I chain-related proteins (MIC) A and B are involved in cellular immune responses to virus infections but their role in respiratory syncytial virus (RSV) infection has not been studied. We aimed to determine how RSV infection modulates IL-15 production, MHC class I and MICA expression in respiratory epithelial cells, the molecular pathways implicated in virusinduced IL-15 production and how interferon (IFN)-c alters RSV-induced IL-15 production and MHC class I and MICA expression.We infected respiratory epithelial cell lines (A549 and BEAS-2B cells) and primary bronchial epithelial cells with RSV and measured production of IL-15, expression of MHC I and MICA and the role of the transcription factor nuclear factor (NF)-kB.We report here that RSV increases IL-15 in respiratory epithelial cells via virus replication and NF-kB-dependent mechanisms. Therefore, IL-15 is likely to play a key role in the immune response to RSV infection but no data are available regarding RSV modulation of IL-15 production and MICA/B expression in human respiratory epithelial cells.We aimed to determine how RSV infection modulates IL-15 production in respiratory epithelial cells and the molecular pathways implicated in virus-induced IL-15 production. In addition, because RSV infection induces a type 1 immune response characterised by increased IFN-c production [11], we determined how IFN-c alters RSVinduced IL-15 production and the levels of MHC class I and MICA molecules in epithelial cells.

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“…Respiratory viruses, especially rhinoviruses, are an important cause of exacerbation and may be isolated in .50% of cases [6]. Rhinoviruses are also the viruses most frequently associated with the common cold [7].…”

mentioning

confidence: 99%

Epidemiological relationships between the common cold and exacerbation frequency in COPD

Hurst

Donaldson²,

Wilkinson³

et al. 2005

Eur Respir J

110

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Higher exacerbation incidence rates in chronic obstructive pulmonary disease (COPD) are associated with more rapid decline in lung function and poorer quality of life, yet the mechanisms determining susceptibility to exacerbation remain ill-defined. The same viruses responsible for common colds are frequently isolated during exacerbations. The current authors hypothesised that exacerbation frequency may be associated with an increased frequency of colds, and investigated whether increased exacerbation frequency was associated with increased acquisition of colds, or a greater likelihood of exacerbation once a cold has been acquired.A total of 150 patients with COPD completed diary cards recording peak expiratory flow, and respiratory and coryzal symptoms for a median 1,047 days. Annual cold and exacerbation incidence rates (cold and exacerbation frequency) were calculated, and the relationships between these variables were investigated.This analysis is based on 1,005 colds and 1,493 exacerbations. Frequent exacerbators (i.e. those whose exacerbation frequency was greater than the median) experienced significantly more colds than infrequent exacerbators (1.73 versus 0.94?yr -1). The likelihood of exacerbation during a cold was unaffected by exacerbation frequency. Patients experiencing frequent colds had a significantly higher exposure to cigarette smoke (46 versus 33 pack-yrs).Exacerbation frequency in chronic obstructive pulmonary disease is associated with an increased frequency of acquiring the common cold, rather than an increased propensity to exacerbation once a cold has been acquired.

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Respiratory viruses in exacerbations of chronic obstructive pulmonary disease requiring hospitalisation: a case-control study

Cited by 487 publications

References 30 publications

Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Pathogen-directed Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

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

Epidemiological relationships between the common cold and exacerbation frequency in COPD

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