1/n- My friends @CyrilPedia and @dpaxorales threw down the gauntlet, yr beloved @germcells went for it: today we will be talking about #COVID19 and testicular damage. The reason: two fresh off the press studies based on COVID-19 autopsies. #infertility
2/n- The first study is by the team of Tiannan Guo in Hangzhou, China. They looked at the proteome of different tissues and noticed a minor effect of COVID-19 infection in the testis. cell.com/cell/fulltext/…
3/n- Out of the total of 5336 significantly dysregulated proteins (compared to controls) found in multiple organs of COVID-19 patients, only 10 were found in the testis. This small number included both germ cell and somatic proteins. 
4/n- Despite these subtle changes, Tiannan's team argues, based on testicular histology, that COVID-19 reduces Leydig cell number and is associated with spermatogenic impairment. Yet, the histology data provided still leaves some room for speculation.
5/n- This is the representative image of a COVID-19 testis (Fig. 7C). Note that the interstitial tissue is poorly preserved (evidenced by the significant lacunae between tubules). This issue can result, by itself, in lower numbers of Leydig cells in the prep.
6/n- The small proteome differences in the testis of COVID-19 patients are an interesting finding, and their possible effect on Leydig cells an exciting possibility. Nevertheless, the physiological consequences of these differences, if any, remain IMO to be fully clarified.
7/n- The second study is by the team of Shuiqiao Yuan in Wuhan, China. nature.com/articles/s4142…
8/n- Here substantial changes were observed at the RNA level between COVID-19 testes and controls: 2645 upreg. and 2789 downreg. RNAs in COVID-19 patients.
9/n- Histology data showed extensive spermatogenic defects in COVID-19 patients (increased germ cell loss and compromised tissue architecture), but not in age-matched controls.
10/n- Importantly, Shuiqiao's team observed scattered infiltration of immune cells in the interstitial tissue of COVID-19 patients, but rarely so in controls.
11/n- And that brings me to my main point: I’m convinced that the spermatogenic impairment phenotypes reported in autopsies of (mostly old) COVID-19 patients are the reflection of a severe systemic inflammatory response rather than a direct effect of the virus on gonadal tissue.
12/n- Even though the ACE2 receptor is expressed in Leydig cells, spermatogonia and Sertoli cells, there is still no definitive evidence directly linking COVID-19 to spermatogenic impairment.
13/n- Indeed, the virus was undetectable (by RT-PCR) in the semen of 34 adult men recovering from COVID-19 one month after diagnosis. fertstert.org/article/S0015-…
14/n- And, in the case of a patient where the virus was actually detected in spermatogenic cells, no obvious testicular abnormalities were detected. researchsquare.com/article/rs-193…
15/15- Those are my 2 cents on the matter, and I’d love to hear about your views (particularly if in disagreement 😅). Peaceout!
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