Risk factors for lower respiratory complications of rhinovirus infections in elderly people living in the community: prospective cohort study

Nicholson, Karl G.; Kent, Julie; Hammersley, Vicky; Cancio, Esperanza

doi:10.1136/bmj.313.7065.1119

Cited by 141 publications

(104 citation statements)

References 34 publications

(39 reference statements)

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“…The definition of lower respiratory tract involvement in the latter studies was less stringent than that defining exacerbation in the present report. Therefore, it is suggested, in agreement with GREENBERG et al [13], that COPD patients as a group are not more susceptible to respiratory viral infections, and, in agreement with NICHOLSON and coworkers [16,17], that patients with COPD do not appear more likely to develop lower respiratory tract symptoms during such events than other elderly subjects. However, the current authors have shown that cold frequency in COPD is variable, and this masks an important effect in frequent exacerbators who do indeed have an increased frequency of colds.…”

Section: Discussionsupporting

confidence: 75%

“…The incidence and clinical features of upper respiratory tract viral infection in community studies of the elderly have been reported by NICHOLSON and coworkers [16,17]. Here, the annual incidence rate was 1.2?patient -1 ?yr -1 , similar to the current data, and, in 63% of patients with documented rhinoviral infections, there was evidence of lower respiratory tract involvement.…”

Section: Discussionmentioning

confidence: 68%

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Epidemiological relationships between the common cold and exacerbation frequency in COPD

Hurst

Donaldson²,

Wilkinson³

et al. 2005

European Respiratory Journal

109

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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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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 68%

Epidemiological relationships between the common cold and exacerbation frequency in COPD

Hurst

Donaldson²,

Wilkinson³

et al. 2005

European Respiratory Journal

109

View full text Add to dashboard Cite

show abstract

“…Overwhelming evidence exists that cigarette smoke is also associated with a significant increase in the risk of respiratory infections, and smoking is associated with both increased prevalence and severity of upper respiratory infections (URIs) (2)(3)(4)(5). Exposure to cigarette smoke is a major risk factor for the development of URIs in children (6), and was identified as a risk factor in lower respiratory tract complications of rhinovirus infection in older adults (7). Furthermore, a recent study found that patients hospitalized because of rhinovirusinduced exacerbations of asthma were significantly more likely to be current smokers than nonsmokers (odds ratio, 11.2) (8).…”

mentioning

confidence: 99%

Cigarette Smoke Decreases Innate Responses of Epithelial Cells to Rhinovirus Infection

Eddleston¹,

Lee²,

Doerner³

et al. 2011

Am J Respir Cell Mol Biol

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Exposure to cigarette smoke is associated with a significant increase in the risk for respiratory viral infections. The airway epithelium is the primary target for both cigarette smoke and respiratory viral infection. We investigated the effects of cigarette smoke on the response of airway epithelial cells to rhinovirus infection. We found that pre-exposure of BEAS-2B cells or primary normal human bronchial epithelial cells (NHBEs) to cigarette smoke extract (CSE) reduced the induction of mRNA of the chemokines CXCL10 and CCL5 by either the viral mimic polyinosine-polycytidylic acid (Poly I:C) or human rhinovirus 16 (HRV-16) infection. The HRV-16-induced release of CXCL10 and CCL5 was also significantly suppressed by CSE. Activation of the IFN mediator STAT-1 and the activation of JNK by poly I:C and HRV-16 were partially suppressed by pre-exposure to CSE. In contrast, the poly I:C-induced and HRV-16-induced phosphorylation of ERK1/2 was unaffected by CSE. HRV-16-stimulated IFN-b mRNA was also significantly reduced by CSE. Because suppression of the IFN response to viral infection was associated with increased viral production, we assessed HRV-16 RNA concentrations. Exposure to CSE resulted in an increase in HRV-16 RNA at 48 hours after the infection of BEAS-2B cells. These data demonstrate that exposure to CSE alters the response of airway epithelial cells to HRV infection, leading to decreased activation of the IFN-STAT-1 and SAP-JNK pathways, the suppression of CXCL10 and CCL5 production, and increased viral RNA. A diminished, early epithelial-initiated antiviral response to rhinovirus infection could contribute to the increased susceptibility of subjects to prolonged respiratory viral infections after exposure to cigarette smoke.

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“…Furthermore, the pathogenic role of HRVs in lower respiratory tract infections of infants, elderly and immunocompromised patients has been reported [6][7][8].…”

mentioning

confidence: 99%

Antibodies induced with recombinant VP1 from human rhinovirus exhibit cross-neutralisation

Edlmayr¹,

Niespodziana²,

Popow‐Kraupp³

et al. 2010

European Respiratory Journal

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Human rhinoviruses (HRVs) are the major cause of the common cold and account for 30-50% of all acute respiratory illnesses. Although HRV infections are usually harmless and invade only the upper respiratory tract, several studies demonstrate that HRV is involved in the exacerbation of asthma.VP1 is one of the surface-exposed proteins of the viral capsid that is important for the binding of rhinoviruses to the corresponding receptors on human cells. Here we investigated its potential usefulness for vaccination against the common cold.We expressed VP1 proteins from two distantly related HRV strains, HRV89 and HRV14, in Escherichia coli. Mice and rabbits were immunised with the purified recombinant proteins.The induced antibodies reacted with natural VP1 and with whole virus particles as shown by immunoblotting and immunogold electron microscopy. They exhibited strong cross-neutralising activity for different HRV strains. Therefore, recombinant VP1 may be considered a candidate HRV vaccine to prevent HRV-induced asthma exacerbations.

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Risk factors for lower respiratory complications of rhinovirus infections in elderly people living in the community: prospective cohort study

Cited by 141 publications

References 34 publications

Epidemiological relationships between the common cold and exacerbation frequency in COPD

Epidemiological relationships between the common cold and exacerbation frequency in COPD

Cigarette Smoke Decreases Innate Responses of Epithelial Cells to Rhinovirus Infection

Antibodies induced with recombinant VP1 from human rhinovirus exhibit cross-neutralisation

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