The Spike Protein, AT1 Receptors and Male Infertility

Spike Protein exposure has demonstrably resulted in increased AT1R antibodies in those suffering from Post-COVID Vaccination Syndrome.

The changes of AT1 concentrations in the testes of normal C57BL/6 mice (A), RAB mice (B), and ± AT1KO mice (C) during the second (○) and fourth weeks (□). Error bar indicates the mean ± SD and significances are indicated as ∗ p < 0.01

One of the most challenging aspects of researching SARS-CoV-2 and its Spike Protein is that so many findings contain conflicting results. In today’s discussion, we look at the sera of post-COVID vaccination controls and those who suffer from post-COVID vaccination syndrome. In the cohort of those suffering from post-COVID vaccination syndrome, we find an increased presence of AT1R antibodies, yet those vaccinated without developing the syndrome have decreased levels.

A subset of eight of the analyzed receptor antibodies differed significantly (p < 0.0001) between post-vaccination sera (6 months after the last vaccination) in the control cohort and post-vaccination sera (>5 months after the last vaccination) of PACVS-afflicted persons. Six of these antibodies (AT1R, ETAR, M2R, M3R, β2-adr-R, MASR) were significantly (p < 0.0001) higher in PACVS subjects than in post-vaccination controls. Coincidentally, these six receptor antibodies exhibited vaccination-associated decreases in controls,

Chronic Fatigue and Dysautonomia following COVID-19 Vaccination Is Distinguished from Normal Vaccination Response by Altered Blood Markers
https://www.mdpi.com/2076-393X/11/11/1642

What the article does not discuss about these antibodies is what we will now discuss. The angiotensin II type 1 receptor mentioned above (AT1R) is a very important receptor. It is a key player in cardiovascular signaling pathways.

The importance of the renin angiotensin aldosterone system in cardiovascular physiology and pathophysiology has been well described whereas the detailed molecular mechanisms remain elusive. The angiotensin II type 1 receptor (AT1 receptor) is one of the key players in the renin angiotensin aldosterone system. The AT1 receptor promotes various intracellular signaling pathways resulting in hypertension, endothelial dysfunction, vascular remodeling and end organ damage. Accumulating evidence shows the complex picture of AT1 receptor-mediated signaling; AT1 receptor-mediated heterotrimeric G protein-dependent signaling, transactivation of growth factor receptors, NADPH oxidase and ROS signaling, G protein-independent signaling, including the β-arrestin signals and interaction with several AT1 receptor interacting proteins. In addition, there is functional cross-talk between the AT1 receptor signaling pathway and other signaling pathways. In this review, we will summarize an up to date overview of essential AT1 receptor signaling events and their functional significances in the cardiovascular system.

AT1 receptor signaling pathways in the cardiovascular system
https://pmc.ncbi.nlm.nih.gov/articles/PMC5607088/

I studied this receptor in the context of knockout. Knockout is when you eliminate the expression of a gene, and I found something very interesting yet disturbing. AT1R has other vital functions, particularly in the reproductive system. When you knockout AT1R in male mice testes, they become infertile. Antibodies binding to a receptor impair its functionality. It can be as if they were “knockedout” since they cannot carry out their normal tasks.

Knocking out AT1R had a dramatic effect on the ability of male mice to reproduce. No females that spent time with the KO males became pregnant, and the sperm was malformed.

The pregnancy rate of female mice was determined in one week of cage closure with male mice in Control and ± AT1KO groups. None of the female mice mated with ± AT1KO male mice became pregnant. Moreover, the pregnancy rate in 2-week normal mice was 50%, and the pregnancy rate in 4-week normal mice was 55% (Table 5). The plasma testosterone levels were detected in these mice but no significant difference was found (data not shown).

The total deformity rate was 59% in ± AT1KO mice, significantly (P < 0.01) higher than those in normal mice (19%) and in ARB mice (25%). Enlarged (fat) head appeared to be the mostly increased deformity in spermatozoa from ± AT1KO mice (201/642, compared to 26/990 in control group and 23/708 in ARB group). Spermatozoa with no hook and folded tails were also significantly increased.

Decreased angiotensin receptor 1 expression in ± AT1 Knockout mice testis results in male infertility and GnRH reduction
https://rbej.biomedcentral.com/articles/10.1186/s12958-021-00805-1

Why is this important? Because we know the Spike Protein mRNA is found in the testes.

Biodistribution of lipid-nanoparticle in rat, Pfizer study November 2020. From TGA FOI reply 2389-6 [5] (p. 45).

‘Spikeopathy’ Part 1: COVID-19 Spike Protein Is Pathogenic, from Both Virus and Vaccine mRNA
https://www.researchgate.net/publication/373210100_'Spikeopathy'_Part_1_COVID-19_Spike_Protein_Is_Pathogenic_from_Both_Virus_and_Vaccine_mRNA

And now we have evidence for something which the NIH has, so far, vehemently denied.

Based on the studies published so far, there is no scientific proof of any association between COVID-19 vaccines and fertility impairment in men or women.

The impact of COVID-19 vaccines on fertility-A systematic review and meta-analysis
https://pmc.ncbi.nlm.nih.gov/articles/PMC9464596/

We now have a mechanism by which Spike Protein mRNA vaccines may indeed cause male infertility. Males suffering from post-COVID Vaccination Syndrome should have fertility tests. We need to determine if this is occurring in humans.

Still, the questions remain. Why does this only happen in some? And, if we are repeatedly exposed to the Spike Protein, will it eventually happen in all?

Thank you, as always, for your dialogue, readership and support.