A previous study by researchers from the University of Miami Miller Scholl of Medicine, Florida-USA had found evidence of the SARS-CoV-2 virus remaining within the endothelial cells of penile tissue as much as seven months after infection, which suggests that direct damage to cavernosal endothelium may affect erectile function.
A past study involving more than 230,000 males had showed that up to 20 percent of men exhibit erectile dysfunction issues after contracting the SARS-CoV-2 virus!
Another study involving the meta-analysis of more than 60 published peer reviewed studies concluded that Erectile Dysfunction affects a large proportion of male population who have been exposed to the SARS-CoV-2 coronavirus.
The study findings were published in the peer reviewed journal: Andrology
Electron microscopy and immunohistochemical staining showed SARS CoV-2 virus in the penile corpus cavernosum of patients 1 month after COVID-19 recovery. Immunohistochemical staining intensity correlated with the severity of previous infection. Transmission electron microscopy revealed intracellular virtual particles of about 80 nm with a typical morphology of prominent spikes and electron-dense dots of nucleocapsid in addition to vesicles filled with virus-like particles.
Cells showed increased membrane trafficking. The 1 month after COVID-19 group showed an increased number of fibroblasts. The 7 months after COVID-19 group had similar morphology and immunoreactivity as control group.
In this report, we provide evidence of COVID-19 in the human penis long after the initial infection. Our study also suggests that endothelial dysfunction from COVID-19 infection can contribute to resultant ED. Vascular integrity is necessary for erectile function, and endothelial damage associated with COVID-19 is likely to affect the penile vascular flow, resulting in impaired erectile function.
We could not detect viral protein in penis tissue by immunohistology, possibly due to comparably low viral RNA load in the penis. This result was not surprising since recent studies show that COVID-19 isolation is unlikely from samples with low RNA loads . H&E staining from our specimens did not show significant results compared to previous studies in which COVID-19 infection caused mild to moderate accumulation of lymphomonocytic inflammatory cells in a perivascular or subendothelial distribution .
Based on the current findings we can draw two hypotheses about how the SARS-CoV-2 virus can lead to the ED. First, similar to other complications related to COVID-19, of ED can be the result of systemic infection resulting in widespread endothelial dysfunction. This is supported by our findings of endothelial dysfunction seen in men with COVID and ED.
Second, we can also hypothesize that the worsening of these patient’s ED can be due to the virus’ presence within cavernosal endothelium itself. This is best supported by our findings with TEM. The primary limitation of this study were the sample size (n=2) and lack of objective quantification of erectile function before and after infection for patients and controls.
For now, history of COVID-19 should be included in the work-up of ED and positive findings should be investigated accordingly. Patients should be aware of the potential complication of post-COVID-19 ED. Any changes observed in erectile function after infection should be followed up with the appropriate specialist for treatment and to help further investigation into the condition. Future studies are needed to validate the effects of this virus on sexual function.
This study is the first to demonstrate the presence of the COVID-19 virus in the penis long after the initial infection in humans. Our study also suggests that widespread endothelial cell dysfunction from COVID-19 infection can contribute to resultant erectile dysfunction. Future studies will evaluate novel molecular mechanisms of how COVID-19 infection can lead to ED.
REFERENCE LINK :https://wjmh.org/DOIx.php?id=10.5534/wjmh.210055