BREAKING! New Study Suggests That SARS-CoV-2 Infections Can Affect Fertility In Females Through Molecular Mimicry And Other Ways!

Yet more alarming data is emerging on a daily basis about the dangerous effects of SARS-CoV-2 coronavirus infections on the human host and this time a new study by researchers from Sheba Medical Center-Israel, University of Bari-Italy, Strasbourg University-France, Sechenov University-Russia and Tel Aviv University-Israel has found that the novel coronavirus could also affect female fertility thought a number of ways including molecular mimicry.

 
The process of egg production by the ovary or oogenesis, involves a complex differentiation program leading to the production of functional oocytes. This process comprises a sequential pathway of steps that are finely regulated. Genetic predisposition and abnormal immune responses are some of the numerous possible causes of female infertility.
 
The issue as to whether SARS-CoV-2 infections can affect fertility has been raised many times due the high expression of ACE2 in the female reproductive tissues, (The entry receptor for SARS-CoV-2) and the potential damage to germline (oocytes) due to the dysfunction of autophagy in COVID-19.
 
Furthermore molecular mimicry may contribute to female infertility by leading to the generation of deleterious autoantibodies, which could also participate to the onset of an autoimmune disease in infected patients.
 
The study team carried out a systematic analysis to improve the understanding of the possible effects of SARS-CoV-2 infection on female fertility using the angle of molecular mimicry as a starting point.
 
The study findings show a number of rather long linear sequences shared by the SARS-CoV-2 proteins and oogenesis-related proteins that might play a role in the production of possibly pathogenic crossreactive autoantibodies. SARS-CoV-2 spike glycoprotein was found to share 41 minimal immune determinants, i.e., pentapeptides, with 27 human proteins that relate to oogenesis, uterine receptivity, decidualization, and placentation. All the shared pentapeptides that the study team identified, with the exception of four, are also present in SARS-CoV-2 spike glycoprotein–derived epitopes that have been experimentally validated as immunoreactive.
 
The study findings were published in the peer reviewed American Journal of Reproductive Immunology.
 https://onlinelibrary.wiley.com/doi/10.1111/aji.13494
 
When as early as February 2020, when Thailand Medical News published a review on a study by Chinese researchers we knew that the SARS-CoV-2 coronavirus could affect male fertility, we were immediately labeled as fake news by a couple of stupid Italian journalists and a bastard American fact- checker that has no qualification in the field of biological sciences nor medicine who was contracted by Facebook termed the article as being fake news! https://www.thailandmedical.news/news/breaking-news!-latest-research-published-by-chinese-scientists-say-coronavirus-might-render-certain-male-patients-infertile
 
Since then numerous studies have emerged confirming that male fertility is indeed affected by SARS-CoV-2 infections and the article is no longer termed as fake news but we did not receive any apologies or compensation form the bastards.
 
The SARS-CoV-2 coronavirus which causes the COVID-19 disease, is well known to cause severe respiratory illness in infected patients.
 
Importantly however, studies have found that it can affect multiple organs like the heart, kidneys, liver and brain as well.
 
Some individuals who have recovered from COVID-19 have been found to develop multisystem inflammatory syndrome leading to inflamed organs and tissues. The impact of COVID-19 on various systems in the body can manifest as long-term side effects.
 
The study team decided to explore the possibility that COVID-19 can also affect the reproductive function in the body especially that of females, which can lead to infertility in infected patients.
 
The study team propounded three ways that SARS-CoV-2 infection can influence the reproductive system and impact fertility:
 
1) Firstly via direct action of SARS-CoV-2 on Angiotensin-converting enzyme -2 (ACE2) receptor. Angiotensin-converting enzyme -2 (ACE2) receptor plays a vital role in various physiological processes. It is present in the kidneys, heart, thyroid, adipose tissue, and the reproductive system (testis, ovaries, uterus, vagina, and placenta). ACE2 has been found to play a role in follicular development, ovulation, luteal degeneration, endometrial changes, embryo development, etc. Evidence suggests that ACE2 also has a vital role in SARS-CoV-2 pathogenesis by facilitating viral entry into host cells. It has been hypothesized that SARS-CoV-2 may act through the ACE2 receptors on the reproductive system and disrupt its functioning.
 
2) Secondly evasion of autophagy in the host cell by SARS-CoV-2 may disrupt oocyte maturity. A critical mechanism of SARS-CoV-2 pathogenesis is the evasion of the autophagic system in the host cell. Autophagy is a self-cleaning process by which a cell removes unwanted debris, malformed proteins, damaged organelles, etc. Both autophagy and oxidative stress have a role in oocyte longevity. Therefore, by disrupting autophagy in host cells, SARS-CoV-2 may impact oocyte maturation and fertility.
 
3. Thirdly via molecular mimicry between the host and SARS-CoV-2 proteins may influence fertility. The amino acid sequences in the proteins of the host cells and SARS-CoV-2 may exhibit similarities. This can result in cross-reactivity of the antibodies produced by the infected patients against SARS-CoV-2, leading to an autoimmune state where their cells are harmed. This condition is called molecular mimicry.  In earlier studies, it was observed that molecular mimicry between hepatitis B virus (HBV) proteins and myelin basic protein in mice leads to the onset of demyelinating diseases after HBV infection.
 
Significantly, molecular mimicry between SARS-CoV-2 proteins and oogenesis-associated proteins may affect reproductive function.
 
The study team decided to explore if molecular mimicry affects fertility in COVID-19 infected patients.
 
The key hypothesis of this study is SARS-CoV-2 proteins share common peptide sequences with the proteins involved in oogenesis resulting in the production of cross-reactive antibodies. These cross-reactive antibodies may result in the onset of autoimmune diseases.
 
It has been known that peptide sequences made of 5 amino acids (pentapeptides) are considered a minimum requirement for inducing peptide-specific antibodies and for provoking antigen and antibody reactions.
These pentapeptides were used as peptide probes for identifying similarities between human oogenesis-associated proteins and spike protein from SARS-CoV-2.
 
The study team used the UniProtKB database to identify eighty-two human oogenesis-associated proteins. These proteins were joined to artificially create a polyprotein. Further, the spike protein from SARS-CoV-2 was divided into pentapeptides. Analysis was performed to assess if the pentapeptides from the spike protein occurred in the polyprotein. If common pentapeptides were identified, they were checked for their immunoreactivity on the Immune Epitope Database.
 
Shockingly it was found that the peptides that occurred in both the human oogenesis-related protein and the SARS-CoV-2 spike protein are immunoreactive. It was found from the analysis that forty-one pentapeptides from SARS-CoV-2 spike protein occurred in twenty-seven human oogenesis-associated proteins. On the Immune Epitope Database, it was found that all of the matching pentapeptides except for two have been identified to be immunoreactive.
 
Hence these finding showed that COVID-19 patients may develop an autoimmune condition that can affect their fertility!
 
Importantly there exist amino acid sequence similarities between human oogenesis-associated proteins and SARS-CoV-2 spike protein which can elicit the production of cross-reactive antibodies.
 
The study team also found that during SARS-CoV-2 infection, there is a possibility of cross-reactive antibodies being produced against various proteins associated with the reproductive system. This can affect fertility and cause disruptions in the reproductive function of the infected patient.  
 
Also alarmingly some of the possible effects of cross-reactive antibodies attacking the human oogenesis-related proteins include; destruction of germ cells, reduction in the size of the testis and ovaries, alterations in the expression of genes associated with sexual dimorphism, aberrations in the reproductive function, lack of sexual maturation, etc.
 
The research team says that the study findings from the present study are preliminary and indicate a possibility that COVID-19 infected patients may develop an autoimmune condition that can affect their fertility.
 
A more detailed research is required to confirm the findings from this study. Further, the presence of autoantibodies against proteins associated with the reproductive system should be assessed in COVID-19 patients.
 
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