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. 2023 Jun 21;20:132. doi: 10.1186/s12985-023-02103-1

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Simplified schematic representation of the main pathophysiological mechanisms of thyroid injury due to COVID-19 infection. SARS-CoV-2 can damage the thyroid gland in a direct and indirect way. Direct toxicity ACE2 and TMPRSS2 on the surface of thyroid follicular cells serve as an entrance gate for the internalization of the virus into the host cells. The same possibly applies to the integrin α_vβ₃, leading to thyroid gland damage. Additionally, it is suggested that the virus can affect the hypothalamus and the pituitary resulting in HPA-axis dysfunction and, thus, thyroid abnormalities. Indirect toxicity: SARS-CoV-2-induced pulmonary and systemic inflammation and innate immune system activation could potentially damage the thyroid gland in an indirect way. Finally, corticosteroids, which are widely used in the management of COVID-19 patients, inhibit pituitary thyrotrope cells and TRH-release. ACE2 angiotensin-converting enzyme 2; COVID-19 Coronavirus disease 2019; HPA-Axis hypothalamic–pituitary–adrenal axis; SARS-CoV-2 severe acute respiratory syndrome coronavirus 2; TMPRSS2 transmembrane serine protease 2; TRH thyrotropin-releasing hormone