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Genomes analysis reveal that SARS-CoV-2 presents unique features: optimal affinity for angiotensin converting enzyme 2 (ACE2) receptor and a polybasic cleavage site at the S1/S2 spike junction that determines infectivity and host range [3-4) Patients with SARS-CoV-2 infection may present symptoms ranging from mild to severe with a large portion of the population being asymptomatic carriers. The most common reported symptoms include fever (83%), cough (82%) and shortness of breath (31%) [5-6]. Patients suffering from chronic respiratory diseases (CRD) such as chronic respiratory failure, asthma, chronic obstructive pulmonary disease (COPD), interstitial lung diseases (ILD), pulmonary hypertension (PH), sarcoidosis or cystic fibrosis (CF), were immediately considered to be at risk of severe forms of COVID-19 [7]. Indeed, COVID-19 is responsible for various respiratory symptoms, from cough with dyspnea to acute respiratory distress syndrome (ARDS) in its most severe presentation [8-9]. In parallel, it has been shown that COVID-19 patients have an increased risk of venous thromboembolic disease [10]. There is concern that the respiratory complications of COVID-19 could be deleterious in patients with prior CRD. [11-12-13] During COVID-19 pandemic, studies mostly demonstrated that COPD was related with worse outcomes. There may be a few reasons why the course of COVID-19 in COPD patients has been worse. Firstly, COPD patients tend to be older and have more comorbidities which may increase COVID-19 severity [14]. Respiratory failure and hypoxemia, which are the most important causes of death in COVID-19 patients, are more common in COPD patients [15]. Although the exact mechanism of acute exacerbation of ILD is not fully understood, the current belief is that it can be caused by numerous triggers, including infection, or it can be idiopathic.(16) It is likely that respiratory infection with COVID-19 could trigger an exacerbation of underlying ILD and result in poor outcomes. There is similar concern regarding the possibility of exacerbation in patients with sarcoidosis, especially those with fibrotic manifestations.(17)
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Marwan Mohammed, lecturer; Reham El Morshedy, lecturer
Data sourced from clinicaltrials.gov
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