Respiratory viral infection in exacerbations of COPD

McManus, Terence; Marley, Anne-Marie; Baxter, Noreen; Christie, Sharon; O’Neill, Hugh J.; Elborn, J. Stuart; Coyle, Peter; Kidney, Joseph C.

doi:10.1016/j.rmed.2008.06.006

Cited by 124 publications

(139 citation statements)

References 22 publications

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“…Viruses may be isolated in up to 45% of exacerbations of severe COPD, either alone or together with bacteria [23]. Viral exacerbations in COPD are likely to be present with fever [24]. The presence of fever was consistently significantly associated with a lower probability of bacterial isolation in our patients, suggesting again that febrile exacerbations are more likely to be related to viruses.…”

Section: Discussionmentioning

confidence: 60%

Sputum colour and bacteria in chronic bronchitis exacerbations: a pooled analysis

Miravitlles

Kruesmann²,

Haverstock³

et al. 2011

Eur Respir J

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We examined the correlation between sputum colour and the presence of potentially pathogenic bacteria in acute exacerbations of chronic bronchitis (AECBs).Data were pooled from six multicentre studies comparing moxifloxacin with other antimicrobials in patients with an AECB. Sputum was collected before antimicrobial therapy, and bacteria were identified by culture and Gram staining. Association between sputum colour and bacteria was determined using logistic regression.Of 4,089 sputum samples, a colour was reported in 4,003; 1,898 (46.4%) were culture-positive. Green or yellow sputum samples were most likely to yield bacteria (58.9% and 45.5% of samples, respectively), compared with 18% of clear and 39% of rust-coloured samples positive for potentially pathogenic microorganisms. Factors predicting a positive culture were sputum colour (the strongest predictor), sputum purulence, increased dyspnoea, male sex and absence of fever. Green or yellow versus white sputum colour was associated with a sensitivity of 94.7% and a specificity of 15% for the presence of bacteria.Sputum colour, particularly green and yellow, was a stronger predictor of potentially pathogenic bacteria than sputum purulence and increased dyspnoea in AECB patients. However, it does not necessarily predict the need for antibiotic treatment in all patients with AECB.

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Section: Discussionmentioning

confidence: 60%

Sputum colour and bacteria in chronic bronchitis exacerbations: a pooled analysis

Miravitlles

Kruesmann²,

Haverstock³

et al. 2011

Eur Respir J

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“…HRV is the most frequent etiological agent of acute upper respiratory tract infections (URIs) (28) and has been associated with severe lower respiratory tract infections (LRIs) with a spectrum of clinical outcomes (13). There is considerable clinical and epidemiologic evidence linking HRV infections to bronchitis, bronchiolitis, pneumonia, and asthma and chronic obstructive pulmonary disease (COPD) exacerbations (8,18,31,46). In addition, HRV-associated wheezing in infancy is predictive of the development of childhood asthma (17).…”

mentioning

confidence: 99%

Infection and Propagation of Human Rhinovirus C in Human Airway Epithelial Cells

Hao¹,

Bernard²,

Patel³

et al. 2012

J Virol

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Human rhinovirus species C (HRV-C) was recently discovered using molecular diagnostic techniques and is associated with lower respiratory tract disease, particularly in children. HRV-C cannot be propagated in immortalized cell lines, and currently sinus organ culture is the only system described that is permissive to HRV-C infection ex vivo. However, the utility of organ culture for studying HRV-C biology is limited. Here, we report that a previously described HRV-C derived from an infectious cDNA, HRV-C15, infects and propagates in fully differentiated human airway epithelial cells but not in undifferentiated cells. We demonstrate that this differentiated epithelial cell culture system supports infection and replication of a second virus generated from a cDNA clone, HRV-C11. We show that HRV-C15 virions preferentially bind fully differentiated airway epithelial cells, suggesting that the block to replication in undifferentiated cells is at the step of viral entry. Consistent with previous reports, HRV-C15 utilizes a cellular receptor other than ICAM-1 or LDLR for infection of differentiated epithelial cells. Furthermore, we demonstrate that HRV-C15 replication can be inhibited by an HRV 3C protease inhibitor (rupintrivir) but not an HRV capsid inhibitor previously under clinical development (pleconaril). The HRV-C cell culture system described here provides a powerful tool for studying the biology of HRV-C and the discovery and development of HRV-C inhibitors.

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“…HMPV shares epidemiological and clinical traits with RSV causing clinical symptoms ranging from upper respiratory tract disease to severe bronchiolitis and pneumonia and may exacerbate chronic obstructive pulmonary disease (6,12,48,51,57,61,73). RSV has been shown to persist in a variety of cells and animal models (10,17,37,60,61,66,72), and infection with RSV has been shown to induce acute and chronic airway disease correlated with pulmonary function abnormalities (23,52).…”

Section: Discussionmentioning

confidence: 99%

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

Liu

Haas

Poore

et al. 2009

J Virol

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Human metapneumovirus (HMPV) has been identified as a worldwide agent of serious upper and lower respiratory tract infections in infants and young children. HMPV is second only to respiratory syncytial virus (RSV) as a leading cause of bronchiolitis, and, like RSV, consists of two major genotypes that cocirculate and vary among communities year to year. Children who have experienced acute HMPV infection may develop sequelae of wheezing and asthma; however, the features contributing to this pathology remain unknown. A possible mechanism for postbronchiolitis disease is that HMPV might persist in the lung providing a stimulus that could contribute to wheezing and asthma. Using immunohistochemistry to identify HMPV-infected cells in the lungs of mice, we show that HMPV mediates biphasic replication in respiratory epithelial cells then infection migrates to neuronal processes that innervate the lungs where the virus persists with no detectable infection in epithelial cells. After glucocorticoid treatment, the virus is reactivated from neural fibers and reinfects epithelial cells. The findings show that HMPV persists in neural fibers and suggest a mechanism for disease chronicity that has important implications for HMPV disease intervention strategies.Human metapneumovirus (HMPV), a recently recognized paramyxovirus in the Pneumovirus genus, was first isolated in 2001 from nasopharyngeal aspirates of young children with respiratory disease (73). HMPV is a ubiquitous and important respiratory pathogen causing upper and lower respiratory tract disease in infants and young children, but infection may also cause disease in the elderly and immunocompromised (15, 26, 38, 45,73,75). It is recognized that severe respiratory viral infections in childhood are associated with the development of asthma later in life (47), and HMPV disease has been implicated as a trigger for bronchiolitis and asthma in infants and young children (38, 45). These features related to HMPV infection can be severe with prolonged recovery times, a feature that is not well understood.HMPV replication initiates in the upper respiratory tract; however, it can spread to the lower airways involving the bronchi, bronchioles, and alveoli. Evidence from experimental infection in cynomolgus macaques indicates that HMPV replication is short-lived and limited to the apical surface of ciliated respiratory epithelial cells (42). However, the various cell types that may be susceptible to HMPV infection are not completely understood. The HMPV G protein is considered to be the principal means for virus attachment to host cells, and F protein is required for penetration mediated by fusion with the plasma membrane (11, 59). Penetration requires proteolytic cleavage of the F protein, incorporation of the viral envelope into the cell membrane, nucleocapsid release into the cytoplasm, and L protein initiation of viral transcription where replication proceeds in the cytoplasm without nuclear involvement (11,59). Virions assemble at the plasma membrane, where inclusion bod...

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Respiratory viral infection in exacerbations of COPD

Cited by 124 publications

References 22 publications

Sputum colour and bacteria in chronic bronchitis exacerbations: a pooled analysis

Sputum colour and bacteria in chronic bronchitis exacerbations: a pooled analysis

Infection and Propagation of Human Rhinovirus C in Human Airway Epithelial Cells

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

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