COVID-19 and bronchial asthma: current perspectives.

Angiotensin converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2), two receptors on the cell membrane of bronchial epithelial cells, are indispensable for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. ACE2 receptor is increased among aged, males, and smokers. As smoking upsurges ACE2 expression, chronic obstructive pulmonary disease (COPD) patients are prone to SARS-CoV-2 infection, and are at a higher risk for severe forms of COVID-19 (coronavirus disease 2019) once infected. The expression of ACE2 and TMPRSS2 in asthma patients is identical (or less common) to that of healthy participants. ACE2 especially, tends to be low in patients with strong atopic factors and in those with poor asthma control. Therefore, it could be speculated that asthma patients are not susceptible to COVID-19. Epidemiologically, asthma patients are less likely to suffer from COVID-19, and the number of hospitalized patients due to exacerbation of asthma in Japan is also clearly reduced during the COVID-19 pandemic; therefore, they are not aggravating factors for COVID-19. Related academic societies in Japan and abroad still lack clear evidence regarding asthma treatment during the COVID-19 pandemic, and recommend that regular treatment including biologics for severe patients be continued.