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. 2023 Feb 16;21:36. doi: 10.1186/s12915-022-01497-8

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© The Author(s) 2023

Open AccessThis 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. 7 — Hypothetical viral and molecular mechanisms of testis infection and damage by SARS-CoV-2. a SARS-CoV-2 (green color) was identified in spermatogonial cells (Spg), Sertoli cells (SC), Leydig cells (LC), infiltrative monocytes (Mono), macrophages (MΦ), spermatocytes (sptc), and spermatids (sptd). Note viral factories in macrophages and spermatogonial cells (green arrows). A direct influence of SARS-CoV-2 in testicular cells hampers ACE2 activity, while activation of mast cells (chymase positive) elevates the levels of angiotensin II (a potent pro-inflammatory molecule) (asterisks). Angiogenic and inflammatory factors can induce the infiltration and activation of mast cells. High levels of angiotensin II, activation of mast cells, and inflammatory factors can activate (polarize) macrophages. The testicular phenotype of COVID-19 patients (fibrosis, vascular alteration, inflammation, tunica propria thickening, Sertoli cell barrier loss, germ cell apoptosis, and inhibition of Leydig cells) can be linked to elevated angiotensin II and active mast cells and macrophages. b Genes network related to angiotensin II, activated mast cells, and macrophages (pink box) extracted from STRING (https://string-db.org/). These three elements upregulate the inflammatory, apoptotic, fibrotic, and vascular genes while downregulating critical seminiferous tubule and Leydig cell genes. Red arrows: upregulated genes; green arrows: downregulated genes; ~: genes upregulated and downregulated depending on the phase