key: cord-0818388-3855rh76 authors: Yonker, Lael M.; Shen, Kunling; Kinane, T. Bernard title: Lessons unfolding from pediatric cases of COVID‐19 disease caused by SARS‐CoV‐2 infection date: 2020-04-03 journal: Pediatr Pulmonol DOI: 10.1002/ppul.24748 sha: d98865894df1efea3621c64666bb7c0c4caa603c doc_id: 818388 cord_uid: 3855rh76 nan The recent coronavirus outbreak, better known at COVID-19 in the United States or novel coronavirus pneumonia in China, has reached pandemic proportions. The illness is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also known as 2019-novel coronavirus (2019-nCoV). With the first adult cases reported in December 2019 in Wuhan, China, pediatric cases followed shortly thereafter with a strong tendency for familial clusters. 1 Interestingly, total numbers of symptomatic pediatric cases lag dramatically behind adult cases suggesting a protective effect of age. 2 As pediatric pulmonologists, we are used to common respiratory viruses. Yet coronaviruses are unfamiliar. The first two human coronaviruses, HCoV-229E and HCoV-OC43 were identified in 1960s and are well-known causes of the common cold. 3 SARS-CoV-2 infection has unique features that offer clues to its underlying biology. The Chinese reports indicate that children are significantly less affected by COVID-19, and when children do develop symptoms, they include fever and dry cough that rarely advance to severe disease. The Chinese Center for Disease Control and Prevention identified 2143 children (aged 0-18 years) with laboratory-confirmed or suspected COVID-19; one death was reported in this group. 4 The most common symptoms are fever (65%) and cough (45%). 5 Up to one-third of reverse-transcription polymerase chain reaction confirmed-positive pediatric patients remain completely asymptomatic. 6 However, 6% of all pediatric patients with COVID-19 developed severe/critical illness, with upwards of 11% of infants under the age of 1 year developing severe/critical disease. 4 Interestingly, the radiographic changes that are characteristic of SARS-CoV-2 infection can also be seen in pediatric patients, even without progress to severe disease. Case series of pediatric patients in various regions of China reported that nearly 50% to 80% of the children had abnormal computed tomography (CT) findings, often displaying ground-glass opacities and nodules, mostly located in the lower lobe of both lungs near the pleural area. [6] [7] [8] Interestingly, one pediatric case series reported the chest CT findings of consolidation with a surrounding halo, suggesting parenchymal infection were seen in 50% of pediatric patients, a finding not previously Immunosenescence, the progressive decline in immune function with increasing age, is a possible explanation. Pediatric patients appear to maintain normal white blood cell counts and lymphocyte counts, 7 while adults often develop abnormalities in neutrophil counts and T-cell depletion. 10 However, the mechanism for this discrepancy is unclear. Alternatively, lessons learned from prior coronavirus infections, namely SARS-CoV, the pathogen responsible for severe acute respiratory syndrome (SARS) outbreak in 2003, have shown than the virus binds to the angiotensin-converting enzyme type 2 (ACE2) receptor to allow viral entry into type II pneumocytes in the lung. As there is homology in the sequence of the receptor-binding domain for the two viruses, it is felt ACE2 receptor is also the site of entry for SARS-CoV-2. 11 As these ACE2 receptors are upregulated in individuals with COPD, hypertension, or smoking history, this may explain why these populations are at increased risk for more severe disease. 8, 12 As pediatric pulmonologists, we are on high alert for our most vulnerable patients with underlying lung disease. Although the overall pediatric numbers are low, rare lung disease in children may not fall into these categories. Cystic fibrosis (CF), for example, is rare in the Chinese population, so how both pediatric and adult CF patients fare with COVID-19 is yet to be seen. In the meantime, we should proceed with caution; optimizing treatments for underlying lung disease seems prudent. Furthermore, minimizing cough related to asthma could reduce the potential aerosolization of the virus in an otherwise asymptomatic carrier. In that same vein, choosing hydrofluoroalkane-inhaler administered medications over nebulizers will also help reduce the aerosolized virus. Focusing on the pediatric population as a means of preventing disease spread is critical. 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