COVID-19 and COPD: a narrative review of the basic science and clinical outcomes

Abstract

The 2019 coronavirus disease (COVID-19) pandemic is caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). Clinical outcomes, including mortality, are worse in males, older individuals and patients with comorbidities. COPD patients are included in shielding strategies due to their susceptibility to virus-induced exacerbations, compromised pulmonary function and high prevalence of associated comorbidities. Using evidence from basic science and cohort studies, this review addresses key questions concerning COVID-19 and COPD. First, are there mechanisms by which COPD patients are more susceptible to SARS-CoV-2 infection? Secondly, do inhaled corticosteroids offer protection against COVID-19? And, thirdly, what is the evidence regarding clinical outcomes from COVID-19 in COPD patients? This up-to-date review tackles some of the key issues which have significant impact on the long-term outlook for COPD patients in the context of COVID-19.

FIGURE 1

The implications of angiotensin converting enzyme (ACE)2 dysfunction during severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection. In the absence of infection, ACE2 is working at capacity and the levels of angiotensin II (ang II) are tightly regulated by conversion to angiotensin 1–7 (ang 1–7). Ang 1–7 activates the Mas receptor to regulate inflammation and vasomotor tone. During SARS-CoV-2 infection, ACE2 activity is reduced due to receptor occupancy, shedding and internalisation and the levels of ang II increase. Ang II activates the AT1 receptor to cause increased pro-inflammatory cytokine production, increased vasoconstriction, increased vascular permeability, oedema and lung injury. Pulmonary inflammation increases and acute severe respiratory failure may ensue.

FIGURE 2

Inhaled corticosteroid (ICS) use in COPD: implications for coronavirus disease 2019. ICS prevent exacerbations in eosinophilic COPD patients, probably in part by targeting type 2 inflammation in these individuals. ICS may have further benefit by reducing the ability of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) to proliferate, and by limiting SARS-CoV-2 cellular entry by reducing angiotensin converting enzyme (ACE)2 expression as a result of inhibiting type 1 interferon (IFN) production. However, immunosuppression may increase susceptibility to respiratory infections leading to secondary bacterial colonisation and increasing the risk for pneumonia in some individuals. ^#: ICS reduces ACE2 expression by reducing type 1 IFN production.

FIGURE 3

Prevalence of COPD among patients with coronavirus disease 2019 with different severity. Data summary from larger patient cohorts (n >1000 for hospitalised patients or >500 for critically ill patients).

FIGURE 4

Impact of COPD on the outcomes of coronavirus disease 2019. Data summary from larger patient cohorts (n >1000 for hospitalised patients or >500 for critically ill patients). ICU: intensive care unit.

FIGURE 5

The key issues addressed by this review. SARS-CoV-2: severe acute respiratory syndrome-coronavirus-2; COVID-19: coronavirus disease 2019; ICS: inhaled corticosteroids; ACE2: angiotensin converting enzyme 2. +: benefits of ICS; −: dangers of ICS.