SARS-CoV-2 infection and its effects on the endocrine system

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing corona virus disease 2019 (COVID-19) can infect multiple tissues, including endocrine organs, such as the pancreas, adrenal, thyroid, and adipose tissue. The main receptor for SARS-CoV-2, ACE2, is ubiquitously expressed in the cells of the endocrine organs and accordingly, the virus has been detected in various amounts in all endocrine tissues in post-mortem samples from COVID-19 patients. The infection with SARS-CoV-2 may directly lead to organ damage or dysfunction, such as hyperglycaemia or in rare cases, new-onset diabetes. Furthermore, an infection with SARS-CoV-2 may have indirect effects affecting the endocrine system. The exact mechanisms are not yet completely understood and have to be further investigated. Conversely, endocrine diseases may affect the severity of COVID-19 and emphasis has to be laid on reducing the prevalence, or enhance the treatment, of these often non-communicable diseases in the future.

Keywords: ACE2; COVID-19; SARS-CoV-2; autoimmune; endocrine; metabolic.

Fig. 1

Factors influencing SARS-CoV-2 entry. When the SARS-CoV-2 spike protein binds to its receptor, the virus is internalized into the host cell. A number of recepors on the host cell have been shown to be involved in direct binding of the SARS-CoV-2 spike protein. However, before that the spike protein is primed by different proteases. The binding between SARS-CoV-2 and its receptor can be stabilized/destabilized. The expression of the main receptor for SARS-CoV-2, ACE2, is regulated by HMGB1.

Fig. 2

Plausible mechanisms of dysregulation in endocrine diseases and COVID-19. There are several reasons why endocrine and especially metabolic diseases may lead to severe progression of COVID-19. One possible cause is the chronic inflammatory responses in the internal adipose tissue. In adipose tissue with overly enlarged fat cells, there is mass production of pro-inflammatory cytokines. In addition, infiltration of immune cells into the adipose tissue is enhanced. These cells produce inflammatory substances themselves, leading to a chronic inflammatory state. Moreover, these inflammatory substances are strongly suspected of contributing to insulin resistance, a precursor of type 2 diabetes. Infection with SARS-CoV-2 under this condition is associated with a high risk of an immune system overreaction, a so-called cytokine storm, which is a potentially life-threatening immune system derailment. Conversely, direct infection with SARS-CoV-2 can lead to organ damage.