In addition, SARS-CoV-2 infection was associated with increased inflammation and activation of programmed cell death pathways in human adrenocortical cells 3, 4. However, no proof of an active replication could be found, indicating that SARS-CoV-2 is passively transmitted through the adrenal vascular system 4. Interestingly, SARS-CoV-2 was also detected in adrenal endothelial cells 4. For example, SARS-CoV-2 RNA and protein were detected in 45% of adrenal glands obtained from patients who died due to a critical course of COVID-19 infection 3. Moreover, these reports provided evidence that SARS-CoV-2 might not only target human adrenocortical cells 3, 4, but might also actively replicate in these cells 4. Several reports, including our own, have confirmed the expression of these receptors in the adrenal gland 3, 4. Susceptible cells also need to express co-receptors required for virus internalization, such as transmembrane protease serine 2 or furins.
To be a target of SARS-CoV-2, cells must express angiotensin-converting enzyme 2, which enables direct binding of virus spike protein to the cell surface. Moreover, adrenocortical cells might undergo programmed apoptotic or necrotic cell death as a consequence of intracellular viral replication 2. In addition, several pathogen-derived toxins might directly affect adrenocortical cell function through binding to toll-like receptors expressed by those cells. These infections are associated with an increased risk of bilateral adrenal gland haemorrhages and inflammation orchestrated by infiltrating immune cells. Adrenal insufficiency is frequently found in patients with meningococcal sepsis, tuberculous adrenalitis and opportunistic viral infections.
Bacterial and viral tropism to adrenal glands is quite common, and certain infections can cause adrenal damage 2.
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