The Possible Dual Role of the ACE2 Receptor in Asthma and Coronavirus (SARS-CoV2) Infection

A new virus belonging to the coronaviridae family has been identified and named severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) (Zhu et al., 2020). This virus can generate a severe respiratory disease named coronavirus disease-2019 (COVID-19). In November 2019, SARS-CoV-2 began to infect humans and cause high rates of respiratory disorders worldwide; accordingly, COVID-19 was declared a pandemic in March 2020 (Li J. Y. et al., 2020). COVID19 has already affected millions of people and killed over 600,000 individuals worldwide (WHO, 2020). Similar to severe acute respiratory syndrome coronavirus-1 (SARS-CoV-1), which was responsible for the 2002 pandemic, SARS-CoV-2 infection is initiated when its S-protein binds to the angiotensin-converting enzyme 2 (ACE2) receptor through which it gains entry into the host’s cells (Kuba et al., 2005; Walls et al., 2020). The affinity of SARS-CoV-2 for the ACE2 receptor is 10 times higher than that of SARS-CoV-1 (Wrapp et al., 2020). This receptor is mainly expressed in the lungs and to a lesser degree in other organs, such as the heart, kidneys, and intestines (Bavishi et al., 2020), which could explain the increased prevalence of lung infection. Many risk factors are associated with the course and severity of COVID-19, including older age, systemic arterial hypertension (SAH), pregnancy, and obesity (Alberca et al., 2020a,b). Although asthma is a debilitating pulmonary syndrome, initial reports have not identified asthmatic patients as having a higher risk for COVID-19 (Guan et al., 2020; Zhang et al., 2020). In this manuscript, we review the possible association between the SARS-CoV-2 entry receptor ACE2 and asthma.