COVID-19 Endothelial Dysfunction Can Cause Erectile Dysfunction


Senior Member

A pilot study to describe histopathological features of penile tissue of patients who recovered from symptomatic COVID-19 infection and subsequently developed severe erectile dysfunction (ED).

Materials and Methods
Penile tissue was collected from patients undergoing surgery for penile prosthesis for severe ED. Specimens were obtained from two men with a history of COVID-19 infection and two men with no history of infection. Specimens were imaged with TEM and H&E staining. RT-PCR was performed from corpus cavernosum biopsies. The tissues collected were analyzed for endothelial Nitric Oxide Synthase (eNOS, a marker of endothelial function) and COVID-19 spike-protein expression. Endothelial progenitor cell (EPC) function was assessed from blood samples collected from COVID-19 (+) and COVID-19 (−) men.

TEM showed extracellular viral particles ~100 nm in diameter with peplomers (spikes) near penile vascular endothelial cells of the COVID-19 (+) patients and absence of viral particles in controls. PCR showed presence of viral RNA in COVID-19 (+) specimens. eNOS expression in the corpus cavernosum of COVID-19 (+) men was decreased compared to COVID-19 (−) men. Mean EPC levels from the COVID-19 (+) patients were substantially lower compared to mean EPCs from men with severe ED and no history of COVID-19.

Our study is the first to demonstrate the presence of the COVID-19 virus in the penis long after the initial infection in humans. Our results also suggest that widespread endothelial cell dysfunction from COVID-19 infection can contribute to ED. Future studies will evaluate novel molecular mechanisms of how COVID-19 infection leads to ED.

Who wants to take a guess about whether other viruses also stick around in the body causing dysfunctions of various parts internal or external? What if no one had bothered to really look before in things like the blood vessels? Because that is POTS and a lot of ME symptoms and AFAIK no one has done this sort of cellular analysis.

So this year we definitely found our viruses don't get wiped out from the body and they stick around causing dysfunctions, hardly the first paper of its type this year. Which virus determines the types of dysfunctions possible and the cells it could infect and where that virus sticks around determines how those possibilities manifest. There are a lot of viruses and a lot of places in the body and that would explain chronic illnesses with families of similarities but a lot of differences in severity and symptoms.


Senior Member
ironically, this long covid symptom will be taken the most seriously and receive the most funding...
I assume the same will prove true of the vaginal wall of women who have had COVID....any studies yet?

I agree that it's possible that Long Covid will overtake us in the way of funding and research. This time we have to be far more proactive than we've been in the past. At the very least, all research material should be extended to our researchers which certainly wasn't done during the AIDS crisis and MS. Both receive extreme amounts of govt. funding, but we have to make ourselves known as much as possible.

This has occurred too many times in the past. We were yesterday's news right from the time CFS/ME/FM/began. I also agree that the name certainly didn't help us, but then I'm not so sure that ME is any better. Can't we come up with something that denotes how serious this is, without scaring people off with a name they can't even
pronounce or spell? Yours, Lenora.
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