Covid male sterility papers + HPV, herpes

as previously discussed:

A recent report published in JAMA Network Open revealed that in an analysis 38 semen samples from COVID-19 patients, 6 (four at the acute stage of infection and, alarmingly, two who were recovering) tested positive for the virus by RT-PCR.1 Importantly, at this point, we have no idea whether the actual virus was viable and infectious. Nevertheless, the possibility that this coronavirus could have a pathophysiological impact on the testes was suggested by additional data indicating that active COVID-19 infection dramatically reduced the testosterone-to-LH ratio, suggesting a significant impact on the responsiveness of Leydig cells to LH stimulation.2 In many ways, we should not be surprised by these observations because the blood-testes barrier is known to offer little defense against viral invasion, given the wide range of pathogenic viruses (HIV, hepatitis, mumps, papilloma) that are known to be capable of damaging the testes and rendering the host infertile.

Furthermore, the spike protein that gives the COVID-19 virus its corona is known to target ACE2 (angiotensin-converting enzyme 2), which is highly expressed by several cell types in the testes including Leydig cells, Sertoli cells, and the germ line. As a result of these factors, several opinion pieces have been published already, raising the possibility of testicular damage and infertility consequent to COVID-19 infection.24 

However, it is also possible that the virus could gain access to male germ cells once they leave the testes, either in the epididymis or following ejaculation. In this Opinion Article, I shall be focusing on this post-testicular route of infection pointing out, for the first time, that the mature spermatozoon has all of the machinery needed to bind this virus, fuse with it, and even achieve reverse transcription of the viral RNA into proviral DNA. Such considerations raise the possibility that spermatozoa could act as potential vectors of this highly infectious disease. This happens in insects5—why not us?


The other side of COVID-19 pandemic: Effects on male fertility


The outbreak of novel coronavirus disease 2019 (COVID-19) has become a major pandemic threat worldwide. According to the existing clinical data, this virus not only causes respiratory diseases and affects the lungs but also induces histopathological or functional changes in various organs like the testis and also the male genital tract. The renin-angiotensin system (RAS), also ACE 2 and TMPRSS2 play an important role in the cellular entry for SARS-CoV-2.

Because the male genital system presents high ACE 2 expression, the importance of this pathway increases in COVID-19 cases. As the COVID-19 pandemic has affected the male genital system in direct or indirect ways and showed a negative impact on male reproduction, this paper focuses on the possible mechanisms underlying the damage caused by COVID-19 to the testis and also other components of the male genital tract.


and they wanna force all young men to get it

college age men too

and all young women

when other papers cite it might act like an STD?



  • The male genital system presents high ACE 2 expression therefore, it will be highly important to investigate and clarify the relationship between COVID-19 and the male genital tract.

I’m not even a man but I can feel my lady balls shrink reading that.

If we look at the mechanisms of these changes caused by SARS-CoV-2 in the testis, as mentioned above, this virus uses ACE 2 for entry into the cells through its surface spike (S) proteins. S proteins have two subunits, S1 and S2, which are responsible for receptor recognition and membrane fusion. Studies have shown that SARS-CoV-2 enters into the host cell through the binding of its C-terminal domain of the S1 subunit to ACE 2. Additionally, some studies have reported that the level of autophagy receptor SQSTM1/p62 in SARS-CoV-2 infected cells has increased, suggesting a decrease in autophagy flux.

So, SARS-CoV-2 itself or via ACE 2 can directly induce or inhibit the autophagy pathway to achieve virus survival.

As a result, SARS-CoV-2 may cause male reproductive disorders by regulating the level of autophagy in male germ cells.4 On the contrary, another hypothesis is that testis degeneration in the COVID-19 cases is attributed to an increase in testicular temperature as an indirect effect of the inflammation.5

or :-

Do the jabs cause inflammation?

Can spike proteins microwave your balls? Do they nuke your little swimmers?


Another molecule effective at entering the cell of the SARS-CoV-2 is host proteases like transmembrane serine protease 2 (TMPRSS2), which cleaves the viral S protein to induce a conformational change that allows to a fusion of the virus and host cell membranes.34 TMPRSS2 is the key molecule for the successful infection process.35 

This protease is more expressed in human tissues than ACE 2; co-expression of ACE 2 and TMPRSS2 has been shown in the testis, endometrium, and placenta. Researchers investigated the coexpression of these two molecules in the testis and accordingly, they found that ACE 2 is predominantly expressed in myoid cells, spermatogonia, Leydig, and Sertoli cells, while TMPRSS2 is expressed in spermatogonia and (elongated) spermatids of the testicular tissue34 (Figure 3).

I warned you about endometriosis-like function. Maybe naturally having endo is protection?

It’s lifelong inflammation. Kinda like cancer. You literally have to cut the tissues out.

Like Fight Club, they’d have to take your balls.

Shocked men aren’t more protective of their bollocks and demanding ONE safety study.

ModRNA has owners. Repossession is plausible, legally.

STD angle:

“Recent studies have reported that SARS-CoV-2 is easily found in human bodily fluids.35 The presence of a virus in a semen sample is still a topic of discussion and research due to the small number of studies. For example, two different studies have analyzed SARS-CoV-2 presence in semen samples and according to these studies, SARS-CoV-2 (+) semen samples were found in two patients from 23 cured patients and four patients from 15 patients in the acute phase. Another study reported that SARS-CoV-2 was not detected in the semen samples of 34 COVID-19 patients.31

“It is also known that the prostate gland secretes prostate fluid, one of the main seminal components, and muscles of the gland help in pushing the seminal fluid through the urethra during ejaculation.31 The critical point is that, as we mentioned above, a small percentage of the prostate hillock and club cells express ACE 220 and also TMPRSS2 is highly expressed by the epithelium of the human prostate;37 so it is more likely to get SARS-CoV-2 infection, which may affect its secretions.31 

These mechanisms could explain  the SARS-CoV-2 (+) semen samples of the studies.23

“If the presence of the virus in semen is definitively proved by studies, assisted reproduction techniques will also be affected. For instance, testing all male patients like HIV or Hepatitis B/C cases, and using appropriate sperm washing techniques, or paying extra attention to sperm freezing for COVID-19 positive patients.35

“Like SARS-CoV-2, most viruses enter the human body through nasal and oral routes, and viral particles may break the blood-brain barrier.” but don’t worry about shedding?

“It has been reported that the brain cells (glial cells and neurons) also express ACE 2 receptors, making them a possible target to induce neuronal death for SARS-CoV-2. Importantly, the central nervous system plays a critical role in endocrine control and spermatogenesis.31 

The Hypothalamic-Pituitary-Gonadal Axis (HPGa) exerts a vital role in reproduction; in other words, HPGa can inhibit the body’s reproductive functions via hormones.3138

We have our mechanism for sterility, people.

Gonadotropin-releasing hormone (GnRH) expressing neurons from the hypothalamus secretes GnRH and it activates the release of the follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland. A low level of GnRH causes a decrease in FSH and LH, resulting in impaired function of the Sertoli and Leydig cells.31 Ma et al.39 showed that COVID-19 patients had significantly higher serum LH levels but decreased testosterone/LH and FSH levels than healthy men, suggesting potential hypogonadism. Taken together, patients with COVID-19 have been found to present a reduced testosterone/LH ratio, indicating possible subclinical damage to male gonadal function.5 Additionally, activation of the HPGa and subsequent alterations in hormone concentrations play a critical role in poor sperm quality.38

Therefore, besides its direct effects on testis, SARS-CoV-2 may affect fertility indirectly via the central nervous system.31

Like a remote control, for your balls.

In conclusion, all preliminary findings mentioned above suggest that the COVID-19 pandemic affects the male genital system in direct or indirect ways and shows a negative impact on male reproductive health, inducing spermatogenic failure. Additional studies are necessary to answer all the questions and further investigations are warranted, but ACE 2 and TMPRSS2 play an important role in the cellular entry for SARS-CoV-2. As the male genital system presents high ACE 2 expression, the importance of this pathway increases in COVID-19 cases.


and onward

Could COVID-19 have an impact on male fertility?


The pandemic caused by Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to several hypotheses of functional alteration of different organs. The direct influence of this virus on the male urogenital organs is still to be evaluated. However some hypotheses can already be made, especially in the andrological field, for the biological similarity of the SARS-CoV and SARS-CoV2. As well as SARS-CoV, SARS CoV-2 uses the ‘Angiotensin Converting Enzyme-2’ (ACE2) as a receptor to enter human cells. It was found that ACE2, Angiotensin (1-7) and its MAS receptors are present, over in the lung, also in the testicles, in particular in Leydig and Sertoli cells. A first hypothesis is that the virus could enter the testicle and lead to alterations in testicular functionality. A second hypothesis is that the binding of the virus to the ACE2 receptor, could cause an excess of ACE2 and give rise to a typical inflammatory response. The inflammatory cells could interfere with the function of Leydig and Sertoli cells. Both hypotheses should be evaluated and confirmed, in order to possibly monitor fertility in patients COVID-19+.

Specific genes relating to male fertility have already been found e.g.

oddly recommended with covid papers?

Male infertility is a rising problem around the world. Often the cause of male infertility is unclear, and this hampers diagnosis and treatment. Spermatogenesis is a complex process under sophisticated regulation by many testis-specific genes. Here, we report the testis-specific gene 1700102P08Rik is conserved in both the human and mouse and highly expressed in spermatocytes. To investigate the role of 1700102P08Rik in male fertility, knockout mice were generated by CRISPR-Cas9. 1700102P08Rik knockout male mice were infertile with smaller testis and epididymis, but female knockout mice retained normal fertility. Spermatogenesis in the 1700102P08Rik knockout male mouse was arrested at the spermatocyte stage, and no sperm were found in the epididymis. The deletion of 1700102P08Rik causes apoptosis in the testis but did not affect the serum concentration of testosterone, luteinizing hormone, and follicle-stimulating hormone or the synapsis and recombination of homologous chromosomes. We also found that 1700102P08Rik is downregulated in spermatocyte arrest in men.

Together, these results indicate that the 1700102P08Rik gene is essential for spermatogenesis and its dysfunction leads to male infertility.

As the incidence and severity of SARS-CoV-2 are reported to be higher in males than females, Shastri et al. performed a study to determine the time to viral clearance after infection in a total of 68 individuals (48 males and 20 females) with median age of 37 years (Shastri et al., 2020).

They observed that females were able to achieve viral clearance significantly earlier than males.

Furthermore, a serial follow-up evaluation of three families with both male and female patients demonstrated that female members of the same household cleared the SARS-CoV-2 infection earlier in each family (Shastri et al., 2020). In order to determine the reason for delayed clearance in males, they also checked the expression of ACE2 in tissue-specific repositories.

It was found that testicular tissues were one of the tissues showing ACE2 expression in 3 independent RNA expression databases (Human Protein Atlas, FAMTOM5 and GETx). Interestingly, the ovarian tissue showed very low expression of ACE2 (Shastri et al., 2020).

so women may be the red herring here

ACE2 and fat study, so expect fatty side effects

Impact of COVID-19 and other viruses on reproductive health

They admit the male HPV link I posted about previously.

Male infertility is linked to some viral infections including human papillomavirus (HPV), herpes simplex viruses (HSV) and human immunodeficiency viruses (HIVs). Almost nothing is known about severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) effect on fertility. The possible risk factors of coronavirus disease 2019 (COVID-19) infection on fertility comes from the abundance of angiotensin-Converting Enzyme-2 (ACE2), receptor entry of the virus, on testes, a reduction in important sex hormone ratios and COVID-19-associated fever. Recent studies have shown a gender difference for COVID-19 rates and comorbidity. In this review, we will discuss the potential effect of COVID-19 on male fertility and talk about what needs to be done by the scientific community to tackle our limited understanding of the disease. On the other side, we will focus on what is known so far about the risk of COVID-19 on pregnancy, neonatal health and the vertical transfer of the virus between mothers and their neonates. Finally, because reproduction is a human right and infertility is considered a health disease, we will discuss how assisted reproductive clinics can cope with the pandemic and what guidelines they should follow to minimise the risk of viral transmission.

Remember, viral entry via SPs cause inflammation that might cause sterility? WELL-

Virus entry begins when the virus surface enzyme called Spike (S) glycoprotein binds to the angiotensin-converting enzyme 2 (ACE2) located on the host cell membrane (Hoffmann et al., 2020; Wang et al., 2020). S protein contains two different domain regions: S1 and S2, each one has its own role in virus entry. S1 domain is the part that binds directly to the host ACE2 receptor while the S2 domain helps the virus to fuse with the target cell membrane using its functional elements (Glowacka et al., 2011; Hoffmann et al., 2020). This process is also mediated by a Transmembrane Serine Protease 2 (TMPRSS2) located on the surface of the target cell membrane used for the priming of the S protein causing the virus entry (Hoffmann et al., 2020; Shen, Mao, Wu, Tanaka, & Zhang, 2017; Wang et al., 2020).

When the fusion of the virus with the target cell membrane occurs, the virus releases its genome and using the host cell organelles to replicates its RNA and releases new mature virion to target other cells (Boopathi, Poma, & Kolandaivel, 2020; Jiang, Hillyer, & Du, 2020) Figure 1.

wait wait wait the wild virus replicates its RNA too?

minor flex –

3.1 Human papillomavirus (HPV) and its impact on male fertility

Human papillomavirus (HPV) is a non-enveloped DNA virus and sexually transmitted worldwide. In some cases, it causes either warts or precancerous lesions (Ljubojevic & Skerlev, 2014). More than 170 HPV types have been identified and completely sequenced (Chouhy, Bolatti, Pérez, & Giri, 2013). Recent studies suggest that HPV infection affects male fertility. In cases of idiopathic asthenozoospermia, HPV DNA was observed in the sperm cells of infertile patients (Foresta et al., 2010; Lee, Huang, King, & Chan, 2002) confirming its role of infertility. Strong association between HPV infection and impairment of sperm parameters, especially a reduction in sperm motility and concentration, was observed in HPV-infected men (Garolla et al., 2012; Jeršovienė, Gudlevičienė, Rimienė, & Butkauskas, 2019). Garolla and coworkers (Garolla et al., 2012) reported that HPV can bind to the head of a spermatozoon and impair sperm motility in men. Certain sperm DNA exons undergo apoptotic fragmentation on HPV-infected men suggesting that HPV types degrade different exons of important genes (Lee et al., 2002). Collectively, these evidences suggest that HPV plays a role in male factor infertility.

3.2 Herpes simplex viruses (HSVs) and their impact on male fertility

Herpes simplex viruses (HSVs) are enveloped DNA viruses of the family Herpesviridae. HSVs include two distinct viruses HSV-1 and HSV-2 (Whitley & Roizman, 2017). HSVs are sexually transmitted and targets reproductive system. HSV-1 causes oral and, occasionally, genital sores while HSV-2 is common cause of genital herpes which may lead to infertility problems in both males and females. HSV DNA was detected in semen from about 50% asymptomatic infertile males (Amirjannati et al., 2014; Bezold et al., 2007; Monavari et al., 2013; Neofytou, Sourvinos, Asmarianaki, Spandidos, & Makrigiannakis, 2009). A strong association of HSV infection and low sperm count, poor motility, and increased apoptotic cells were reported (Monavari et al., 2013). Haematospermia and a lower seminal volume and abnormal viscosity were found in HSV-2-infected males which indicate prostate dysfunction (Kurscheidt et al., 2018). Bezold et al. (2007) reported significantly reduced sperm concentration and motility as well as reduced citrate concentrations and neutral α-glucosidase in HSV-infected males, suggested impaired epididymal and prostate function.

The manwhore diseases are listed alongside HIV, lol.
The wages of sin is death, in men as well as women.
How will PUAs recover? They won’t. God Willing.

The concern show that SARS-CoV-2 may affect male reproductive organ and thus results in male infertility stems from several observations. Early studies both in China and Italy showed that males are more susceptible to COVID-19 compared to females (Guan et al., 2020; Livingston & Bucher, 2020).

A recent large cohort observational study from United Kingdom featuring around 20 thousands COVID-19 patients reported that males represented 60% of cases and considered the male sex as one of the risk factors for COVID-19 (Docherty et al., 2020).

DS: MRAs: crickets

More alarming is the result of a new systematic review—included 48 recently published articles and 16 databases—where it found that men are more likely to suffer or to die from the complications of COVID-19 compared to women (Serge, Vandromme, & Charlotte, 2020).

DS: suffer or die? Binary?

Large proportion of these vulnerable males is in their childbearing age, and thus their reproductive ability can be affected.

Finally, like influenza, COVID-19 patients suffer from fever, which may affect sperm production. It was reported that febrile illnesses had an impact on semen parameters (Sergerie, Mieusset, Croute, Daudin, & Bujan, 2007). Total sperm count and motility percentage were reduced significantly at days 15, 37 after fever episode before going back to normal after several weeks (Sergerie et al., 2007). Increase of sperm DNA fragmentation index and alteration in the nuclear protein composition of ejaculated spermatozoon were reported after fever episode (Evenson, Jost, Corzett, & Balhorn, 2000).

Different viruses use different routes to enter into the host cells. SARS-CoV-2 uses the same ACE2 receptor used by its cousin, the SARS-CoV virus, with the help of TMPRSS2 (see Figure 1). Single cell expression analysis has detected the expression of ACE2 RNA not only in the lung epithelial cells, but also in several other organs, among them are the kidneys and the bladder (Fan et al., 2020; Lin et al., 2020; Tipnis et al., 2000). Protein expression analysis also confirmed the presence of ACE2 protein in multiple tissues (Hamming et al., 2004).

Interestingly, the highest expression of ACE2 was found in the testes (Fan et al., 2020). The high expression of the ACE2 receptor in the testes raises a concern that the SARS-CoV-2 has the route to enter some if not all testicular cells and thus could cause damage.

To further analyse the types of testicular cells vulnerable for SARS-CoV viruses, Wang et al. studied single-celled ACE2 expression in the human testes (Wang & Xu, 2020). They found that ACE2 is mainly expressed in spermatogonia, leyding and Sertoli cell, while spermatocytes and spermatids had very low expression (Wang & Xu, 2020). Interestingly, TMPRSS2 expression is similar to ACE2, where TMPRSS2 was also enriched in spermatogonia and spermatids. It has been also shown that ACE2 positive spermatogonia cells express genes that are important for virus reproduction and transmission, while ACE2 positive leyding and Sertoli cells express genes that are required for cell–cell junctions and immunity.

Collectively, these results highlight the risk of COVID-19 on testicular cells and on the spermatogenesis process.

The only direct evidence for the effect of COVID-19 on male reproductive function comes from a study where sex hormones namely testosterone (T), luteinising hormone (LH) and follicle-stimulating hormone (FSH) among others were compared between COVID-19 patients and healthy controls. While the T level was not different between the two groups, the ratio of T to LH and the ratio of FSH to LH were significantly decreased in COVID-19 patients (Ma et al., 2020).

This might be the first direct evidence for the influence of COVID-19 on testicles’ ability to produce sex hormones; however, the results of this study should be followed by a more direct analysis of the seminal fluid of COVID-19 patients to evaluate the effect—if any—on sperm count, volume, morphology or motility. It has been reported that SARS-CoV causes orchitis in addition to other complications (Xu et al., 2006), so it is also possible that SARS-CoV-2 may cause the same complication in males.


And it may kill pregnant women only:

Pregnant women have been shown to be at high risk of comorbidity and mortality related to influenza infections (Rasmussen, Jamieson, & Bresee, 2008; Rasmussen, Jamieson, & Uyeki, 2012). The previous SARS infection showed that pregnant women had higher fatality rate (25%) compared to the general population (10%; Wong et al., 2004). With the rise of numbers of pregnant women and children affected by COVID-19, it is worth to know if pregnant women are a high-risk group for COVID-19 death or increased hospitalisation and also to evaluate the risk of vertical transfer either from the mother to the foetus or from the neonates to the mother.

Neonatal health is another important concern in the COVID-19-infected mothers. In a study from Wuhan, 33 neonates were born to mothers with COVID-19, and no health complications were reported except for shortness in breath in four cases (Zeng et al., 2020). Other studies, including less number of cases, did not report any neonatal health issues except for low birthweight (<2,500 g) and premature delivery (Cao et al., 2020; Chen & Lou, 2020). Two other studies from China and Iran reported two neonatal deaths out of 19 cases studied (Hantoushzadeh et al., 2020; Zhu, Wang, et al., 2020). No cases of miscarriages have been reported in the first trimester of COVID-19 pregnancies. Overall, it seems that neonates delivered by COVID-19 pregnant mothers have no increased risk of clinical complications compared to normal pregnancies and some of the reported neonatal complications could be related to mothers’ overall health status rather than a consequence of COVID-19 infection.

Then why jab them?

The risk of vertical transfer of SARS-CoV-2 between the mother and the foetus is possible knowing that the ACE2 receptor is expressed in the placenta and uterus (Levy et al., 2008); however, most published data do not support this predication as most neonates born for mothers affected by COVID-19 tested negative (Chen et al., 2020; Liu et al., 2020; Yu et al., 2020). A few studies have reported a vertical transfer of SARS-CoV-2 from the mother to the neonates (Hantoushzadeh et al., 2020; Yu et al., 2020), but these studies should be carefully interpreted as they occur less frequently and possibly resulted because of the neonatal exposure to SARS-CoV-2 after delivery.

One way to get you on the hook financially is reproductive tech.

Risk of ovarian hyperstimulation syndrome should be taken very seriously during COVID-19 pandemic crisis and all guidelines clearly stated that reproductive endocrinologists should adopt gonadotropin-releasing hormone (GnRH) antagonist as a default protocol for ovarian stimulation with GnRH-agonist trigger to minimise the risk of ovarian hyperstimulation syndrome (OHSS), hospital admissions and intensive care unit (ICU) occupancy (ASRM; Carugno et al., 2020ESHREJSF).

Isn’t that an endometriosis fertility treatment? Odd. So you’re saying it works?

Many health issues related to COVID-19 have been addressed in this review. Pregnancy and maternal health have been discussed. Many reports have evidences against a direct link between COVID-19 and maternal death. Neonates born to a COVID-19 mothers are not at increased risk of adverse health consequence compared to the ones born for COVID-19-unaffected mothers, and the possibility of viral vertical transfer has not been confirmed. Large cohort studies should be followed to confirm these results; additionally, first-trimester COVID-19 cases should be included and be evaluated for the risk of miscarriages.

The gender difference in COVID-19 incidence, comorbidity and death rates—males are at higher risk—requires prompt actions to understand the source of difference biologically and behaviourally. Viral infection by HPV, HSV, HIVs, HBV, HCV and MuV challenges reproductive health and can be considered as a risk factor for male infertility. These viruses have been detected in semen and can impair testicular function. Some viruses such as HIV, MuV and SARS-CoV are associated with orchitis resulting in male infertility, so it would be interesting to study if SARS-CoV-2 can cause the same problem. Because many males at childbearing age are affected by COVID-19, the high expression of ACE2 receptor in the testes and the association of COVID-19 with fever; a multidimensional andrological translational research project was suggested (Salonia et al., 2020). This project aims to develop international collaboration for data registry, hormonal studies and genomic studies to better understand the sex difference for COVID-19 health-related consequences.

re the endo treatment

GnRH agonists are a group of drugs that have been used to treat women with endometriosis for over 20 years [1]. They are modified versions of a naturally occurring hormone known as gonadotropin releasing hormone, which helps to control the menstrual cycle.

At present, the usual length of treatment with a GnRH agonist is 3–6 months. However, in Germany, 12 months treatment with add-back therapy (5 mg of norethisterone per day) has been approved, and other countries may do the same in the future.

The sperm allergy vaccine and genocide by sterilisation

Missed this nugget.

Provoking an allergic reaction to…. one’s own sperm?

Why do under-30s “need” anything, let alone a random new ‘vaccine’ with no ingredients list available?

1995 evidence of precedent for deceptive vector of transmission, official contamination reportage and hence, UN contravention of genocide law established in the 1940s, section (d) and (c):

“PIP: A priest, president of Human Life International (HLI) based in Maryland, has asked Congress to investigate reports of women in some developing countries unknowingly receiving a tetanus vaccine laced with the anti-fertility drug human chorionic gonadotropin (hCG). If it is true, he wants Congress to publicly condemn the mass vaccinations and to cut off funding to UN agencies and other involved organizations. The natural hormone hCG is needed to maintain pregnancy. The hormone would produce antibodies against hCG to prevent pregnancy. In the fall of 1994, the Pro Life Committee of Mexico was suspicious of the protocols for the tetanus toxoid campaign because they excluded all males and children and called for multiple injections of the vaccine in only women of reproductive age. Yet, one injection provides protection for at least 10 years. The Committee had vials of the tetanus vaccine analyzed for hCG. It informed HLI about the tetanus toxoid vaccine. HLI then told its World Council members and HLI affiliates in more than 60 countries. Similar tetanus vaccines laced with hCG have been uncovered in the Philippines and in Nicaragua. In addition to the World Health Organization (WHO), other organizations involved in the development of an anti-fertility vaccine using hCG include the UN Population Fund, the UN Development Programme, the World Bank, the Population Council, the Rockefeller Foundation, the US National Institute of Child Health and Human Development, the All India Institute of Medical Sciences, and Uppsala, Helsinki, and Ohio State universities. The priest objects that, if indeed the purpose of the mass vaccinations is to prevent pregnancies, women are uninformed, unsuspecting, and unconsenting victims.”


“Vaccines are under development for the control of fertility in males and females. This review discusses developments in anti-fertility vaccines at the National Institute of Immunology, New Delhi, India. A single injection procedure for the sterilization or castration of male animals depending on the site at which the injection is given, has passed through field testing and is expected to be on the market in the near future. Vaccines inducing antibodies against the human chorionic gonadotropin have gone through phase I trials with satisfactory results. A vaccine producing a consistently bioeffective antibody response against gonadotropin-releasing hormone is ready for phase I/II clinical trials in patients of carcinoma of prostate after due experimentation in animals and toxicology studies. Research to identify sperm antigens for incorporation into second generation vaccines is in progress.”

Control, like farm animals. Single injection for castration of male animals possible.

Look forward to the “drop of testosterone levels”. At least you got to drink some bitch tits beer with the ‘boys’. Don’t come crying to me. You wanted to be ‘male animals’.

They want to sterilise you (hCGβ)

It isn’t just Mark of the Beast, the Satanists want to sacrifice all your children, including potential. All count to Moloch.

The Mark is also a marker of infertility. Mark(er) of the Beast (whose sacrifice is what).

You know, owned infertility, like a pet. The Bible says never to get tattoos, and your duty on this earth is to be fruitful and make godly children. Scroll for just studies but context is important, I feel.

HCG-beta sterilises women (and children), what’s the bet it’ll be in one dose of one mandatory thingey, eventually?  As you’ll see, all it needs is one. It mimics fatal cancer, encouraging the body to shut down reproduction to struggle to fight it off. Maybe not the first dose officially to force you all, better space it out to avoid suspicion.
I wonder where they’ll put this, along with other sterilising agents? Mistakes were made, woops! You can’t sue!
Am I crazy now? I’m only covering HCG-beta today, 101 style. Do your own damn research and share share share the studies, 4chan, 8kun, the works.

Sterilization programme imminent like Bill and others did in Nigeria (and other places). Then again with HPV (which reduces fecundity, when checked with age-peers) as previously covered by me.

“The fear of vaccines: Fear that a vaccine used by the WHO to combat polio can cause sterility in both men and women, has spurred some Northern Nigerian states to block a crucial vaccination campaign that is aimed at eradicating the disease from West Africa. “

And you call Africa dumb? They’re not.
Herd immunity is a myth, also covered by me, even at 100% “coverage” (impossible) doesn’t work (unfalsifiable, fake science).
Remember, most spanish flu dead were vaccinated soldiers (and nurses), that’s why it got so many young people.
A pawpaw tested positive for this, FFS. A fruit and a goat!
They never say in ‘outbreaks’ of measles etc, how many who got sick ALREADY HAD the vaccine (most), they’ll deflect or try to hide that topic.

“Efforts to produce a contraceptive vaccine targeting human chorionic gonadotropin (hCG) face several important challenges.”

A ‘vaccine’ to stop you from reproducing. Don’t believe me?

Journal of Reproductive Immunology:
“Gonadotropin-releasing hormone/human chorionic gonadotropin β based recombinant antibodies and vaccines”

Vaccines have been developed against both GnRH and hCG and these have undergone Phase I/II clinical trials documenting their safety, reversibility and efficacy. The heterospecies dimer hCG vaccine prevented pregnancy in women of proven fertility without impairment of ovulation or derangement of menstrual regularity and bleeding profiles.”

Jump through their evil hoops and they might let you be a free human again. Keep reproduction free! Also, end medical segregation. Slaves weren’t allowed to breed until their master said so.

Anti-fertility vaccines, you only naturally express it when you have ‘advanced’ cancer.

“Ectopic expression of hCG/hCGβ is observed in many advanced stage cancers of various origins.”

Mandatory? Medical Marxism argument: I can violate your body with bio-rape implants because it may possibly help me, theoretically – or some hypothetical person.


“These reduce serum testosterone to castration levels causing atrophy of the prostate.”


The prize is disappointment. No lollipop.
“Castration levels” you couldn’t make it up. Evil has a PhD.

Guessing atrophy is permanent? Sounds kinda permanent.
Linked to ‘adverse prognosis’ (death).

Expression of the free β-subunit of human chorionic gonadotropin (hCGβ) in malignant tumors is frequently associated with aggressive disease. The pretreatment serum concentration of hCGβ is an independent prognostic variable in renal cell carcinoma (RCC). The three so-called type II genes (hCGβ 3/9, 5, and 8) have been shown to be up-regulated in relation to type I genes (hCGβ 6/7) in some malignant tumors.”

“This vaccine consists of a synthetic peptide representing, the carboxy-terminal 37 amino acids of hCG beta subunit coupled to diphtheria toxoid. The immunogen is pre- pared by linking the peptide to the carrier using a bifunctional reagent (6-maleimido caproic acyl N- hydroxy saccinimide ester)is in a manner to achieve predictable…”

Search engine (DDG) description:

“The second candidate vaccine is oLH.hCG-TT/CHB: a-subunit of ovine LH associated with hCG, linked to carriers such as TT or cholera toxin chain B (CHB). The third vaccine preparation is a physical mixture of hCG and oLH, each linked to carriers. These vaccines have completed phase I clinical trials in five centres in India.”

1989 publication date.


When you click:

Vaccines are under development for the control of fertility in males and females. This review discusses developments in anti-fertility vaccines at the National Institute of Immunology, New Delhi, India. A single injection procedure for the sterilization or castration of male animals depending on the site at which the injection is given, has passed through field testing and is expected to be on the market in the near future. Vaccines inducing antibodies against the human chorionic gonadotropin have gone through phase I trials with satisfactory results. A vaccine producing a consistently bioeffective antibody response against gonadotropin-releasing hormone is ready for phase I/II clinical trials in patients of carcinoma of prostate after due experimenation in animals and toxicology studies. Research to identify sperm antigens for incorporation into second generation vaccines is in progress.

This, in 1989. I didn’t exist then. Imagine what they have now.

Calling white people (or any) ‘females’ and ‘males’ is dehumanizing, especially intended to destroy you/r genetic lineage. Your God-given right. It just so happens black men recently popularised this use in rap, which isn’t controlled by a certain group with certain investments, is it? Phew.

They want you allergic to your own body. Autoimmune infertility, sterilization by antibody, it’s right there. CASTRATION, CHEMICAL CASTRATION.

A single injection procedure for the sterilization or castration of male animals”

It relates to cancer vaccines

Anti-fertility vaccine again

“Peptides representing the amino acid sequence of the carboxy‐terminal of the human chorionic gonadotropin (HCG) beta subunit were used in studies to determine whether an immunogen could be prepared that would be suitable for an HCG antifertility vaccine. Peptides of varying length were conjugated to several macro‐molecular carriers, in varying peptide‐carrier ratios…”

Chemical human neuter sounds so cruel.

They think they own you.

Target for cancer therapy, apparently? Nice excuse. Sounds so comfy, philanthropy.

WHO knows?

“The World Health Organisation (WHO) Task Force on Birth Control Vaccines has selected the pregnancy hormone human chorionic gonadotropin (hCG) as a target molecule for a contraceptive vaccine.”

You didn’t wanna breed, right?
How much would you pay for an anti-anti-fertility vaccine?
Task Force on Birth Control Vaccines….. selected…. target… fucking Nazi ‘eugenics’ again.

Christians are up first.

They later changed the name for being too obvious on a scale of really fucking obvious to taking le piss. Henceforth, it has become really fucking obvious.

“Over the past 18 years, the WHO Task Force on Vaccines for Fertility Regulation has been supporting basic and clinical research on the development of birth control vaccines directed against the gametes or the preimplantation embryo.”

So including chemical abortion, like the Pill.

18,years, as of writing, totally off the cuff.


NO SHIT, THAT’S THE TITLE. They think they own you.

During 1986-1988, the WHO Special Programme of Research, Development and Research Training in Human Reproduction used the diphtheria toxoid as a carrier for a fragment of the human chorionic gonadotropin (hCG) molecule (a conjugate immunogen) and an immunostimulant in a phase I clinical trial of this prototype antifertility vaccine in sterilized women. Between 1990 and 1991, it conducted teratology studies in rats and rabbits to determine whether the vaccine causes fetal abnormalities. The vaccine did not adversely affect either the animals or their fetuses. Clinical trials of the vaccine’s effectiveness (phase II trials) are scheduled for 1992. At least 2 injections several weeks apart, are needed to produce an anti-hCG immune response which is only effective for 3-6 months, however. So the same components of the original vaccine were placed in a polymer to deliver the vaccine slowly over a prolonged and predetermined time frame. WHO hoped that this advanced vaccine would raise effective immunity levels long enough to last for at least 1 year after 1 injection. WHO is conducting dose-response and toxicity studies of this prototype vaccine in rabbits and baboons to identify the optimal dose which would elicit an effective immunity level over a desired period of time and would be safe for testing in humans. WHO hopes to begin a phase I clinical trial with this advanced anti-hCG vaccine in late 1992. WHO anticipates that the preclinical and clinical trials will reveal a need for further modifications and improvements. WHO is supported multicenter research on antitrophoblast vaccines which target membrane cells of the preimplantation embryo since 1985. It uses monoclonal antibodies (MABs) and recombinant DNA technology to identify and isolate surface molecules. So far this research has tested 15,000 MABs but is centering on 9 MAbs. A study in baboons showed that 1 MAB reduced fertility, even though researchers could only use minute amounts of the protein in the injection.

Population control = PR for genocide. Go after the guidestones people and their love of carving stone.

PR is rebranded propaganda to the post-war period, rebranded deliberately by the likes of one Bernays. That is historical fact.

“Vaccines based on hCG have been proposed as a means either to prevent metastatic cancr6 or to control fertility’. Approaches to development of such vaccines have been pursued usij either the complete beta sub unit of hCG (hCG-fl) or the 37 amino acid CTP alone”

Most people wouldn’t want an anti-cancer anything if it made them sterile.

“The WHO Task Force on Vaccines for Fertility Regulation. Its formation, objectives and research activities”

“As a result of this inter national, collaborative effort, a prototype anti-HCG vaccine is now undergoing clinical testing, raising the prospect that a totally new family planning method may be available before the end of the current decade.”

Guess the year. Guess. I’ll tell you in a few lines.*
“Immunization to regulate fertility…”
“produced by placental cells”

*It’s 1991 published above re WHO. 
PDF here:

save save save

bookmark, usb, email, any way you can get this all out there

This one is tricksy.

“Even though the idea of a birth control vaccine was gaining traction

… WHO task force trial undertaken on women in Sweden testing the vaccine …”

described in SEO brief

paywalls should be illegal

maybe you can find this paper on the piratebay of academic papers

No excuses. Weird they hide this recent one re Swedish info, because it’s ongoing?

Published 1997.

Contesting claims on the safety and acceptability of anti-fertifity vaccines

spellings are often deliberate to thwart SEO

Contesting claims on the safety and acceptability of anti-fertility vaccines


This paper describes the controversy surrounding anti-fertility vaccines, focusing on the antihCG vaccine. It deals first with the rationale that researchers give for the development of antifertility vaccines, and the specific requirements that they set for the new contraceptive method.
Two distinct prototypes of anti-hCG vaccines are clearly emerging, one of which might be
characterised as maximising safety and the other as maximising efficacy. A vocal group of
women’s health advocates have opposed the development of both prototype vaccines, pointing to
theoretical health risks and the potential for abuse, and call for a stop to further research. This
paper shows how the scientists’ discourse on safety and acceptability of the technology to future
users has changed in response to the critique of women’s health advocates. Finally, it reflects on
the role of women’s health advocates in contraceptive technology development, and the
responses of researchers to their actions.

They took over womens’ groups to avoid discussion of important issues.

TLDR trust the “scientists” what human ‘error’? let alone ‘evil’ trust the ‘experts’

you know, pre-replication crisis

scientists often own stock so….. null appeal


The possibility of a contraceptive vaccine targeting human chorionic gonadotropin has long been recognized, but never fully realized.

weird, previously they’ve claimed success in ‘trials’?

they think you’re stupid

you can’t ban something they claim doesn’t exist (yet)

Here we describe an epitope-specific approach based on immunogenic display of hCG-derived peptides on virus-like particles of RNA bacteriophage. A number of recombinant VLPs were constructed, each displaying a different hCG-derived peptide. Some were taken from the disordered C-terminal tail of the hormone, another came from an internal loop, and yet another was an epitope mimic produced by affinity-selection on an hCG-neutralizing antibody target. Immunization of mice with some VLPs yielded antisera that bound the hormone and neutralized hCG biological activity.”

neutralised, like a threat
neutered you – like a dog

share share share the studies, you don’t have to link to me just SHARE

I haven’t posted this previously to avoid it getting censored prematurely.
Is anyone else keeping a tally of how many times I can piss off the WHO or NWO people without being murdered? Just me?

Vice celebrates the self-sterilizing

We should be paying them. One-time lump fee. Just enough for a great holiday.
Weed out the high time preference. £4-5k? Conditional on their signature that they’ll never try to reverse it or otherwise breed, or at least won’t take welfare if/when they do.

If they aren’t responsible enough to make this choice at 18, they aren’t responsible enough to consent to sex. The schools should be blamed, since they were nowhere else.

Please make this the hot new trend.

It’s still eugenics if they do it to themselves.

Congratulations Roosh and the other genetic suicides, you’re in the fine company of these lovely ladies.

“Life isn’t just about reproduction.”

Thank you for not breeding.

cool nothing shocks me scientist indiana jones calm haha amused

I bet the majority were already sterile due to undiagnosed STDs.

As one guy put it “your mutations end with you!”

Essentially they’re recognizing their existence is a mistake of nature.

Tell me Peter Pan Syndrome isn’t a thing.

What would they say to people who think 19, or even 29, is too young to make a decision so final? That this is a narcissistic lifestyle choice designed to hold onto their not-quite adult status? 

Katelin assuredly disagrees.


“I want time alone, time with my partner and time to travel and spend money on luxury. And I don’t think there’s anything wrong with that,” she says.

how is that not-

“My generation live in a broken world. We come from broken homes and have broken minds and bodies. Many of us just don’t want to reproduce. It’s my life, and I’m not hurting anyone.

Still a vector for sexual diseases though, huh?

Never mention that?

They never want other tissues and nerves cut, no, that’s crazy!

superman drinking give up nope

Super-gonorrhea will have a long time to incubate in these people, before spreading to the normal population.

Scientific paper on the depopulation efforts


Medicine and public health are compromised by the highest echelons of science, industry and public administration for the geopolitical objectives of international cohabitation, preservation of resources, environmental conservation and decarbonization, all of which hinge on depopulation. Under the cover of reproductive health involuntary sterilizations are implemented throughout the developing world through adulterated vaccines, while in the developed world flu immunization programs weaken the immune systems of the old and civil servants to shorten lifespans and spare governments from meeting insolvent health care and pension plan obligations in the last stage of the demographic transition. Endocrine disruptors inserted in the basic elements of life to presumably prevent caries chronically subvert the human reproductive system to lower the total fertility rate of every country to replacement level. In the name of sustainable development, experimental carbon capture and sequestration methods as well as solar radiation management methods double as weapons against longevity by subjecting billions to unnaturally high exposure levels of heavy metals so the world’s decarbonization goals are tackled from two directions, by reducing greenhouse gases in the atmosphere and increasing morbidity and mortality among the general population to proactively lower future emissions. Poverty and hunger are used as fronts for the deployment of GMO crops that purportedly increase yields, improve nutrition and require fewer fertilizers and pesticides, but that in fact misuse the latest bioengineering advances to cause subfertility, immune deficiencies and crop failures and thus lower the population by limiting births and increasing deaths. Unless stopped, this engineered genocide will damage the genetic and intellectual endowment of humanity and cause population collapse within 20 years, time during which the incidence and severity of NCDs will grow exponentially irrespective of health system investments and medical breakthroughs. Only a political solution can restore our health as individuals and as a civilization.

The feminists won’t touch forced sterilization programmes but the Guardian has reported on it.

And it happens here too thanks to the SS.

A mother-of-six with learning difficulties can be lawfully forced to be sterilised by authorities to prevent further pregnancies, a judge has ruled.

Health officials and social services bosses made the request to force entry into her home and detain her with “necessary restraint” to be able to carry out sterilisation.

If the authorities don’t like you, they’ll call you disabled and sterilize you.

Some examples of specific learning difficulties are:
  • Dyspraxia

  • Dyslexia

  • Attention Deficit Hyperactivity Disorder (ADHD)

That’s right, we have legal precedent to sterilize practically anyone. On the basis of the opinion of government agents.