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Unravelling airway infection in COPD
S13 Differentiated human rhinovirus loads in stable COPD and at exacerbation
  1. S N George,
  2. A J Mackay,
  3. A R C Patel,
  4. R J Sapsford,
  5. D S Garcha,
  6. G C Donaldson,
  7. J A Wedzicha
  1. University College London, London, UK

Abstract

Introduction Human rhinoviruses (HRV) are the main aetiological agents of virus-associated COPD exacerbations (Seemungal et al, 2001). However the importance of the level of viral load as a trigger for naturally occurring exacerbations is not fully understood. We aimed to assess and quantify HRV prevalence and load in stable and exacerbating patients from the London COPD cohort.

Methods A real-time qPCR protocol was utilised to detect HRV presence and quantify load in sputum samples taken at baseline (n=58) and at COPD exacerbation onset (n=57). COPD patients were defined as stable if exacerbation-free for at least 42 days since the previous exacerbation and more than 14 days before the next. Exacerbations were defined using our usual symptom criteria; an increase in respiratory symptoms for two consecutive days, with at least one symptom being a major symptom; dyspnoea, sputum purulence or volume and the other a major or minor symptom; wheeze, cold sore throat, and cough (Anthonisen criteria). A χ2 test was used to compare HRV prevalence of the two disease phases, and an independent-samples t test was used to compare the differences in viral load.

Results Sixty-four patients provided 115 sputum samples: mean age 70.5 years (SD±8.1); FEV1 45.8% predicted (±20.0%); current smoker 31.3%. There is a significantly higher prevalence of HRV at exacerbation onset, 31.6% (18/57) compared to baseline 15.5% (9/58) (p=0.042). Similarly, the mean viral load was significantly greater at exacerbation onset 1.70 (±1.67) log10 pfu/ml than baseline 0.30 (±0.69) log10 pfu/ml (p=0.025), exhibiting a 25-fold increase in viral load from baseline to exacerbation. 6.9% (4/58) of patients were positive for HRV at baseline only, 26.3% (15/57) at exacerbation only and 8.8% (4/45) at both time points (p=0.006).

Conclusions HRV load is significantly greater at COPD exacerbation than when detected in the stable state. This emphasises the importance of HRV as a key trigger of COPD exacerbations. HRV can be detected in the stable state; however the loads are very low suggesting asymptomatic carriage rather than chronic infection.

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