The SARS-CoV-2 infects the human testes, lower testosterone and can be sexually transmitted from severe COVID-19 survivors

A new study from Brazil looked at the devastating effects of the SARS-CoV-2 virus on testicular tissues among men who had severe COVID-19. [1]

Study subjects

The research examined eleven non-vaccinated male patients who died from COVID-19 complications. They are aged 63.9 ± 13.11 and were admitted to the ICU due to severe pulmonary symptoms. 

The standard treatment at the ICU included antibiotics, antimycotics, invasive mechanical ventilation, hemodialysis, and others. (No ivermectin, vitamin D3, or hydroxychloroquine mentioned).

All patients had children except one. None presented with scrotal symptoms or complaints during their hospital stay, nor did their clinical history reveal previous testicular disorders.

The most prevalent comorbidities were hypertension (nine cases), diabetes mellitus (six), and obesity (six). The testicles were collected no later than three hours after the patients’ death with the families’ consent.

Six COVID-negative patients who underwent orchiectomy due to prostate cancer suspicion serve as the control group for comparison. These patients did not go through any treatment at the time of orchiectomy.

The study was conducted by several authors from Brazil and the US and was very detailed. Their study SARS-CoV-2 infects, replicates, elevates angiotensin II, and activates immune cells in human testes. The study is a preprint at medRxiv and is not yet peer-reviewed but it is the first to show the following findings.

Results

The high SARS-CoV-2 can infect the testis. 

The testicular tissue, just like the respiratory tract, has many ACE2 receptors where the SARS-CoV-2 attaches to begin cell entry and infection. Macrophages and spermatogonial cells, the precursors of sperm cells, are the main SARS-CoV-2 lodging sites and where new virions form. 

One mode of SARS-CoV-2 entrance into the testes is by infected macrophages.

Infected macrophages compromise the “immune privilege” of the testis. The immune privilege allows antigens or “foreign proteins” in an area. Usually, the immune system does not tolerate foreign proteins as they are seen as invaders. 

The testes have the immune privilege because of haploid genes. Haploid genes in the sperm cells contain only half of the chromosome, and the other half will come from the female egg during fertilization. Since haploid genes have only half of the chromosomes, they look like foreign proteins.  

Once the immune privilege of the testes is compromised, the immune system acts on the testes, causing inflammation and scarring, potentially compromising reproductive health. 

SARS-CoV-2 prefers infection and replication in the spermatogonia and macrophages.

Sperm cells mature from spermatogonia. SARS-CoV-2 infected sperm cells raise the potential for sexual transmission of COVID-19. 

The virus remains infective after a prolonged infection in the testes. The study also found that the SARS-CoV-2 maintains its replicative and infective abilities long after the patient’s illness, suggesting that the testes may serve as a viral sanctuary.

Typically, the COVID-19 virus is undetectable 6-12 days after the COVID symptoms start.  In one patient who died 26 days after the symptoms, the SARS-CoV-2 viruses isolated from him were able to infect cell cultures.

The SARS-CoV-2 were detected using gold nanosensors functionalized with anti-spike and anti-nucleocapsid receptors.

High levels of angiotensin II and activated mast cells and macrophages are critical in promoting all testicular alterations.

ACE2 is more than a receptor. ACE2 degrades the angiotensin II hormone. After the SARS-CoV-2 binds to the ACE2, the ACE2 cannot degrade angiotensin II, and angiotensin II  levels go up.

High levels of angiotensin II cause excessive inflammation that is harmful to any cell.  

The longer and more severe the COVID-19, the lower the number of surviving germ cells that mature to become sperm cells raising concerns about infertility.

The intratesticular testosterone levels are 30 times reduced. The lower testosterone is from:

1. The reduction of the Leydig cells that produce testosterone
2. Inflammation from mast cells 
3. High levels of angiotensin II
4. Excessive inflammation from cytokines produced by macrophages inhibits testosterone production.

Testosterone is essential for fertility, sperm maturation, and other health benefits. 

The prevalent types of collagen present in SARS-CoV-2 mediated testicular fibrosis.

Inflammation in the testes can replace functional cells with scar tissue, and thus testosterone and normal sperm maturation are compromised. 

More studies need to be conducted to reproduce the findings of the study.

It should be mentioned that not all men who get COVID-19 will become infertile. A study of 120 participants who had recovered from a proven COVID-19 infection aged 34.7± 9.1 years (range, 18–69 years), with a mean body mass index (BMI) of 24.7 ± 4.4 kg/m². 11 (9.2%) fitting the diagnosis of obesity (BMI>30) showed that sperm quality was estimated to recover after three months. [2].

The same study [2] did not detect SARS-CoV-2 RNA in the semen. However, they only used RT-PCR to detect the SARS-CoV-2 RNA and not the nanosensors used by Costa and colleagues [1]

Take away message

Severe COVID-19 among men can compromise fertility and testosterone production, leading to low libido, impotence, increased breast size, brittle bones, poor concentration, irritability, and depression.

Men who survive severe COVID-19 have the potential to transmit COVID sexually.

This article emphasizes the importance of early COVID-19 treatment for eradicating the virus. Some strains, like the Omicron, can evade vaccine-induced immunity, which is why all should get early treatment for COVID-19.

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