SARS-CoV-2 infection in patients with thyroid disease: a cross-sectional study.

Abstract

The SARS-CoV-2 virus has significantly impacted certain susceptible populations, leading to higher rates of morbidity and mortality, and poorer outcomes for various comorbidities (1). The main risk factors for severe infection and worse disease outcomes include the presence of multiple comorbidities (cardiovascular disease, hypertension, diabetes, and chronic respiratory disease), male gender, and older age (1). The virus is known to utilize the angiotensin-2-converting enzyme (ACE2) and transmembrane protease serine 2 (TMPRSS2) to gain entry into type II pneumocytes in human lungs (2). Interestingly, studies have noted higher levels of ACE2 and TMPRSS2 expression in the thyroid gland (3). It was recently proposed that cleavage of the SARS-CoV-2 spike protein by the furin enzyme is key to this process (4). Thyroid hormone (T3) may interfere with furin expression in the lungs hindering SARS-CoV-2 infectivity (4). However, T3 is also an important pro-inflammatory regulator in immune response during infections (4). As such, we conducted an epidemiological study to evaluate the correlation between thyroid disease and COVID-19 infection rates and severity.