Huge death count this autumn from ADE and cytokine storms?
These SARS-CoV vaccines all induced antibody and protection against infection with SARS-CoV. However, challenge of mice given any of the vaccines led to occurrence of Th2-type immunopathology suggesting hypersensitivity to SARS-CoV components was induced. Caution in proceeding to application of a SARS-CoV vaccine in humans is indicated.
The emergence of the disease SARS and the rapid identification of its severity and high risk for death prompted a rapid mobilization for control at the major sites of occurrence and at the international level. Part of this response was for development of vaccines for potential use in control, a potential facilitated by the rapid identification of the causative agent, a new coronavirus –. Applying the principles of infection control brought the epidemic under control but a concern for reemergence naturally or a deliberate release supported continuation of a vaccine development effort so as to have the knowledge and capability necessary for preparing and using an effective vaccine should a need arise. For this purpose, the National Institute of Allergy and Infectious Diseases supported preparation of vaccines for evaluation for potential use in humans. This effort was hampered by the occurrence in the initial preclinical trial of an immunopathogenic-type lung disease among ferrets and Cynomolgus monkeys given a whole virus vaccine adjuvanted with alum and challenged with infectious SARS-CoV . That lung disease exhibited the characteristics of a Th2-type immunopathology with eosinophils in the lung sections suggesting hypersensitivity that was reminiscent of the descriptions of the Th2-type immunopathologic reaction in young children given an inactivated RSV vaccine and subsequently infected with naturally-occurring RSV –. Most of these children experienced severe disease with infection that led to a high frequency of hospitalizations; two children died from the infection , , .
The conclusion from that experience was clear; RSV lung disease was enhanced by the prior vaccination. Subsequent studies in animal models that are thought to mimic the human experience indicate RSV inactivated vaccine induces an increased CD4+ T lymphocyte response, primarily of Th2 cells and the occurrence of immune complex depositions in lung tissues , , . This type of tissue response is associated with an increase in type 2 cytokines including IL4, IL5, and IL13 and an influx of eosinophils into the infected lung; , , , . Histologic sections of tissues exhibiting this type of response have a notable eosinophilic component in the cellular infiltrates. Recent studies indicate that the Th2-type immune response has both innate and adaptive immune response components , .
In addition to the RSV experience, concern for an inappropriate response among persons vaccinated with a SARS-CoV vaccine emanated from experiences with coronavirus infections and disease in animals that included enhanced disease among infected animals vaccinated earlier with a coronavirus vaccine . Feline infectious peritonitis coronavirus (FIPV) is a well-known example of antibody-mediated enhanced uptake of virus in macrophages that disseminate and increase virus quantities that lead to enhanced disease , . Antigen-antibody complex formation with complement activation can also occur in that infection and some other coronavirus infections in animals. Thus, concern for safety of administering SARS-CoV vaccines to humans became an early concern in vaccine development.
As a site proposed for testing vaccines in humans, we requested and were given approval for evaluating different vaccine candidates for safety and effectiveness. Two whole coronavirus vaccines, one rDNA-expressed S protein vaccine and a VLP vaccine prepared by us were evaluated in a Balb/c mouse model, initially described by others, of SARS-CoV , . The concern for an occurrence of lung immunopathology on challenge of mice vaccinated with an inactivated virus vaccine, as reported by Haagmans, et al. for ferrets and nonhuman primates, was seen by us after challenge of mice vaccinated with a SARS VLP vaccine . This finding was duplicated in an experiment reported here and was also seen in mice vaccinated with a range of dosages of a double-inactivated whole virus vaccine (DIV) and an rDNA S protein vaccine (SV) although the immunopathologic reaction appeared reduced among animals given the S protein vaccine when compared to those given the whole virus vaccine. In later experiments, these findings were confirmed and the vaccine utilized by Haagmans, et al. was also shown to induce the immunopathology in mice. Thus, all four vaccines evaluated induced the immunopathology; however, all four also induced neutralizing antibody and protection against infection when compared to control challenged animals.
In these various experiments alum was used as an adjuvant and this adjuvant is known to promote a Th2 type bias to immune responses . However, the immunopathology seen in vaccinated–challenged animals also occurred in animals given vaccine without alum. In an effort to determine whether an adjuvant that induced a bias for a Th1-type response would protect and prevent the immunopathology, we initiated an experiment where the DI PBS suspended vaccine was adjuvanted with Freund’s complete adjuvant, a Th1-type adjuvant. However, this experiment was aborted by the September, 2008, Hurricane Ike induced flood of Galveston, Texas. An experiment with a SARS-CoV whole virus vaccine with and without GlaxoSmithKline (GSK) adjuvant ASO1 in hamsters has been reported . This adjuvant is thought to induce Th1-type immune responses . The authors indicate no lung immunopathology was seen among animals after challenge, including the group given vaccine without adjuvant; however, whether the hamster model could develop a Th2-type immunopathology is uncertain. Finally, a number of other studies of vaccines in animal model systems have been reported but presence or absence of immunopathology after challenge was not reported.
A summary of the SARS-CoV vaccine evaluations in animal models (including the current report) that indicated an evaluation for immunopathology after challenge is presented in Table 2. As noted all vaccines containing S protein induced protection against infection while the studies with VEE and vaccinia vector containing the N protein gene only did not. Also shown is that a Th2-type immunopathology was seen after challenge of all vaccinated animals when evaluation for immunopathology was reported except the study in hamsters with a GSK whole virus vaccine. Thus, inactivated whole virus vaccines whether inactivated with formalin or beta propiolactone and whether given with our without alum adjuvant exhibited a Th2-type immunopathologic in lungs after challenge. As indicated, two reports attributed the immunopathology to presence of the N protein in the vaccine; however, we found the same immunopathologic reaction in animals given S protein vaccine only, although it appeared to be of lesser intensity. Thus, a Th2-type immunopathologic reaction on challenge of vaccinated animals has occurred in three of four animal models (not in hamsters) including two different inbred mouse strains with four different types of SARS-CoV vaccines with and without alum adjuvant. An inactivated vaccine preparation that does not induce this result in mice, ferrets and nonhuman primates has not been reported.
This combined experience provides concern for trials with SARS-CoV vaccines in humans. Clinical trials with SARS coronavirus vaccines have been conducted and reported to induce antibody responses and to be “safe” , . However, the evidence for safety is for a short period of observation. The concern arising from the present report is for an immunopathologic reaction occurring among vaccinated individuals on exposure to infectious SARS-CoV, the basis for developing a vaccine for SARS. Additional safety concerns relate to effectiveness and safety against antigenic variants of SARS-CoV and for safety of vaccinated persons exposed to other coronaviruses, particularly those of the type 2 group. Our study with a VLP SARS vaccine contained the N protein of mouse hepatitis virus and Bolles, et al., reported the immunopathology in mice occurs for heterologous Gp2b CoV vaccines after challenge . This concern emanates from the proposal that the N protein may be the dominant antigen provoking the immunopathologic reaction.
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.2–4
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
RECONCILE ABOVE WITH
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.
SO THE SPIKE PROTEIN ALONE TARGETS ACE2, FOUND IN THE BALLS, LIKE URINE* (*THAT PART WAS A JOKE)
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
Do the jabs cause inflammation?
Can spike proteins microwave your balls? Do they nuke your little swimmers?
BUT WAIT. THERE’S MORE.
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.
“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.31, 38“
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.
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.
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).
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.
Y NO DO THIS ON JABBEES?
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., 2020; ESHRE; JSF).
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 . 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 SARS-CoV-2 spike protein disrupts the cooperative function of human cardiac pericytes – endothelial cells through CD147 receptor-mediated signalling: a potential non-infective mechanism of COVID-19 microvascular disease
paper DECEMBER 2020
AKA they KNEW
(they knew and they pushed it on you – and your kids, soon!)
Findings We show, for the first time, that the recombinant S protein alone elicits functional alterations in cardiac PCs. This was documented as: (1) increased migration, (2) reduced ability to support EC network formation on Matrigel, (3) secretion of pro-inflammatory molecules typically involved in the cytokine storm, and (4) production of pro-apoptotic factors responsible for EC death. Furthermore, the S protein stimulates the phosphorylation/activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) through the CD147 receptor, but not ACE2, in cardiac PCs.
Accordingly, the neutralization of CD147, using a blocking antibody, prevented the activation of ERK1/2 and partially rescued the PC function in the presence of the S protein.
SO do they permit this treatment to their loyal pets?
I think you’ll find the storms fully operational by the time flu season arrives. AKA Coof Coof Part Two. Satanist humour is killing everyone scared enough of death to get guinea pigged. Great way to sort wheat from chaff actually.
Interpretation Our findings suggest the new, intriguing hypothesis that the S protein may elicit vascular cell dysfunction, potentially amplifying, or perpetuating, the damage caused by the whole coronavirus. This mechanism may have clinical and therapeutic implication.
Where is the evidence that viruses cause disease? I have been asking for almost 12 months now, and no one has been able to provide me with a single peer reviewed journal article showing an isolated virus causes disease. It should be so easy to look through the literature and find a study in a couple of minutes, yet no one seems to be able to do such a thing.Scientists and doctors have already done countless experiments to try and prove germ theory over the course of 120+ years, and all have failed….
In March of 1919 Rosenau & Keegan conducted 9 separate experiments in a group of 49 healthy men, to prove contagion. In all 9 experiments, 0/49 men became sick after being exposed to sick people or the bodily fluids of sick people. https://jamanetwork.com/jour…/jama/article-abstract/221687
In November 1919, 8 separate experiments were conducted by Rosenau et al. in a group of 62 men trying to prove that influenza is contagious and causes disease. In all 8 experiments, 0/62 men became sick. Another set of 8 experiments were undertaken in December of 1919 by McCoy et al. in 50 men to try and prove contagion. Once again, all 8 experiments failed to prove people with influenza, or their bodily fluids cause illness. 0/50 men became sick. In 1919, Wahl et al. conducted 3 separate experiments to infect 6 healthy men with influenza by exposing them to mucous secretions and lung tissue from sick people. 0/6 men contracted influenza in any of the three studies. https://www.jstor.org/stable/30082102?seq=1…
In 1920, Schmidt et al conducted two controlled experiments, exposing healthy people to the bodily fluids of sick people. Of 196 people exposed to the mucous secretions of sick people, 21 (10.7%) developed colds and three developed grippe (1.5%). In the second group, of the 84 healthy people exposed to mucous secretions of sick people, five developed grippe (5.9%) and four colds (4.7%). Of forty-three controls who had been inoculated with sterile physiological salt solutions eight (18.6%) developed colds. A higher percentage of people got sick after being exposed to saline compared to those being exposed to the “virus”. https://pubmed.ncbi.nlm.nih.gov/19869857/https://catalog.hathitrust.org/Record/102609951
In 1921, Williams et al. tried to experimentally infect 45 healthy men with the common cold and influenza, by exposing them to mucous secretions from sick people. 0/45 became ill. https://pubmed.ncbi.nlm.nih.gov/19869857/
In 1924, Robertson & Groves exposed 100 healthy individuals to the bodily secretions from 16 different people suffering from influenza. The authors concluded that 0/100 became sick as a result of being exposed to the bodily secretions. https://academic.oup.com/…/article…/34/4/400/832936…
In 1930, Dochez et al. attempted to infect a group of men experimentally with the common cold. The authors stated in their results, something that is nothing short of amazing. “It was apparent very early that this individual was more or less unreliable and from the start it was possible to keep him in the dark regarding our procedure. He had inconspicuous symptoms after his test injection of sterile broth and no more striking results from the cold filtrate, until an assistant, on the second day after injection, inadvertently referred to this failure to contract a cold. That evening and night the subject reported severe symptomatology, including sneezing, cough, sore throat and stuffiness in the nose.
The next morning he was told that he had been misinformed in regard to the nature of the filtrate and his symptoms subsided within the hour. It is important to note that there was an entire absence of objective pathological changes”. https://pubmed.ncbi.nlm.nih.gov/19869798/
Addendum: One question that frequently comes up is the old story of giving ‘infected blankets’ to the Native Americans to kill them. This story is a cover-up for the real killer which was again allopathic medicine and their vaccines. The proof is in plain sight as always. They vaccinated them. They got sick from the poisoning and died.
“That which can be asserted without evidence can be dismissed without evidence. The onus is on those making the claims that viruses exist to prove they exist. I just finished reading all the books of Charles Fort where we get the word ‘Fortean’ from and he wrote this about germ theory. Keep in mind Governments have known for over 200 years that the germ theory is false: “Of all germ-distributors, the most notorious was Dr Arthur W. Waite, who, in theyear 1916, was an embarrassment to medical science. In his bacteriological laboratory, he had billions of germs. Waite planned to kill his father-in-law, John E. Peck, 435 Riverside Drive, New York City. He fed the old man germs of Diptheria, but got no results. He induced Peck to use a nasal spray, in which he had planted colonies of the germs of tuberculosis. Not a cough. He fed the old man calomel, to weaken hisresistance. He turned loose hordes of germs of typhoid, and then influenza. Indesperation, he lost all standing in the annals of distinctive crimes, and went common, or used arsenic. The old-fashioned method was a success. One’s impression is that, if anything, diets and inhalations of germs may be healthful.” Charles Fort
December 7th 1994 Hollywood Roosevelt Hotel, Greensboro, N.C., Dr Willner (a medical doctor of 40 years experience) an outspoken whistleblower of the AIDS hoax. In front of a gathering of about 30 alternative-medicine practitioners and several journalists, Willner stuck a needle in the finger of Andres, 27, a Fort Lauderdale student who says he has tested positive for HIV. Then, wincing, the 65-year-old doctor stuck himself. In 1993, Dr. Willner stunned Spain by inoculating himself with the blood of Pedro Tocino, an HIV positive hemophiliac. This demonstration of devotion to the truth and the Hippocratic Oath he took, nearly 40 years before, was reported on the front page of every major newspaper in Spain. His appearance on Spain’s most popular television show envoked a 4 to 1 response by the viewing audience in favor of his position against the “AIDS hypothesis.” When asked why he would put his life on the line to make a point, Dr. Willner replied: “I do this to put a stop to the greatest murderous fraud in medical history. By injecting myself with HIV positive blood, I am proving the point as Dr. Walter Reed did to prove the truth about yellow fever. In this way it is my hope to expose the truth about HIV in the interest of all mankind.” He tested negative multiple times. He died of a Heart attack 4 months later 15th April 1995 (yeh right, funny how these naysayers all die suddenly.) – note: people like Princess Di KNEW they weren’t contagious
Severe acute respiratory syndrome coronavirus (SARS-CoV) is a highly pathogenic emergent virus which replicates in cells that can express ABH histo-blood group antigens. The heavily glycosylated SARS-CoV spike (S) protein binds to angiotensin-converting enzyme 2 which serves as a cellular receptor. Epidemiological analysis of a hospital outbreak in Hong Kong revealed that blood group O was associated with a low risk of infection. In this study, we used a cellular model of adhesion to investigate whether natural antibodies of the ABO system could block the S protein and angiotensin-converting enzyme 2 interaction. To this aim, a C-terminally EGFP-tagged S protein was expressed in chinese hamster ovary cells cotransfected with an alpha1,2-fucosyltransferase and an A-transferase in order to coexpress the S glycoprotein ectodomain and the A antigen at the cell surface. We observed that the S protein/angiotensin-converting enzyme 2-dependent adhesion of these cells to an angiotensin-converting enzyme 2 expressing cell line was specifically inhibited by either a monoclonal or human natural anti-A antibodies, indicating that these antibodies may block the interaction between the virus and its receptor, thereby providing protection. In order to more fully appreciate the potential effect of the ABO polymorphism on the epidemiology of SARS, we built a mathematical model of the virus transmission dynamics that takes into account the protective effect of ABO natural antibodies. The model indicated that the ABO polymorphism could contribute to substantially reduce the virus transmission, affecting both the number of infected individuals and the kinetics of the epidemic.
Nearly 85% of all human beings have RH positive blood. Which merely indicates that their red blood cells contain a substance called the RHesus (rhesus) blood factor. Simply put, their positive blood contains a protein that can be linked to the Rhesus monkey.
It is acknowledged that blood factors are transmitted with more exactitude than any other human or animal characteristic. It is not generally known from where the negative RH factor derived, although tantalizing evidence exists that it arrises from genetic experimentation a little over 5,000 years ago.
The highest concentration of RH negative blood occurs in the Basque people of Northern Spain and Southern France, and in the Eastern/Oriental Jews. Only 15% of the entire world´s population is known to have the RH negative blood factor.
While it is known that RH negative blood – (type ‘O’) is the purest blood known to mankind, it is not known from where the negative factor originates, as it is generally theorized by evolutionists that there is an unbroken bloodline from early human prototypes (pre-humans) to present day human beings.
As previously mentioned, ‘Rh negative’ blood indicates no protein connections exist to the Rhesus monkey, whereas ‘RH positive’ blood does carry protein linked to the Rhesus monkey – hence the ‘RH’ designation, ie. rhesus. All other earthly primates have this RH factor. Thus if all humans evolved from that line, all would have the RH factor. Obviously, that is not the case. Therefore, there must have been some manner of intervention giving rise to Rh-negative blood groups.
Blood type ‘O’ is the most common of the blood groups. When we separate the ‘O’ types into ‘negative’ and ‘positive’ we find that ‘O’ negative (the universal donor blood) constitutes less than 7% of the world´s population. Science at this very time is attempting to create a synthetic RH negative ‘O’ blood, but without success. For while the protein in positive blood can be cloned, that of negative blood cannot – which is quite interesting, and may be indicative of an alien origin, or more probable, from early genetic experimentation during previous advanced human civilization(s).
alien? no, God
If the RH negative factor does not derive from any known earthly link (seemingly outside of the theorized evolutionary process) – from where did it originate? Geneticists generally claim the RH-negative factor is a mutation of unknown origin which apparently happened only a few thousand years ago. These ´negative´ blooded people spread heavily into the area of what is now Spain, England, Ireland, France and later into America, Canada and Australia. Basque peoples contain the largest concentration of known ‘O’ negative blooded people today because, they for the most part, have confined themselves to one area, whereas the Celtic people have branched out among all of the new world.
Explains targeting England. Disagree about Celts.
No solid scientific explanation exists as to how or why Rh- blood came about. It is presumed to be the result of a random mutation. Have you ever felt you were weird or different? It may be due to your DNA … 85% of humans have the monkey gene (RH+) and 15% do not (RH-) and maybe have an alien gene instead. RH- people are characterized by higher IQs, sensitive vision, lower body temperatures, sensitivity to heat and sunlight, psychic power, ability to stop watches and electrical appliances and having extra vertebrae. This film explores the possibility that we were bred as a slave race for labor, since 97% of our genetic code is disabled, with only 3% left for us to survive.
So maybe they’re culling o- or…. sparing them? Due to IQ.
no such thing as junk DNA it’s epigenetic
Interestingly, popular sciences endeavor to attribute Rh-neg blood groups to “mutations.” A solid alternative case may be extended to the conclusion that Rh-neg is NOT a mutation, but possibly the original human blood group. This, however, does not reflect tenured thought, and thus has never been adequately researched.
That there was a group of “pure” humans, not directly related to the evolutionary processes on Earth, is a distinct possibility. This reasoning would suggest that the original humans on our planet were not directly related to the apes, but at some point were “MADE” or “genetically engineered” to give such impression.
Perhaps it was never intended that the Rh-positives become the dominant species. That through some as yet undetermined epoch, the genetically impure group gradually became the controlling species, except for several remote enclaves, initiated a wide-ranging genocidal pogrom, effectively wiping out those who gave birth to them.
Maybe the depopulation lot think they’re evening the odds. RH+ babies harm Neg mothers right?
What if effects are type mediated?
I can see why China wanted to kill us.
As you can see the vast majority of RH- people come from the Basque people of France and Spain, and then Europe has the second highest percentage. We can surmise that the RH- blood type originates out of Europe and has spread over to other countries that contain European ancestry heritage. The RH- recessive alleles (+/-) make up approximately 60% of the Basque people and 40% of the Europeans, so that means that a higher percentage of RH+ people in Europe are carrying the genetics of the RH- factor in their DNA.
The Basque people of Spain and France have the highest percentage of Rh negative blood. About 30% have (rr) Rh negative and about 60% carry one (r) negative gene. The average among most people is only 15%-Rh negative, while some groups have very little. The Oriental Jews of Israel, also have a high percent Rh negative, although most other Oriental people have only about 1% Rh negative. The Samaritans and the Black Cochin Jew also have a high percentage of Rh negative blood, although again the Rh negative blood is rare among most black people.
Somehow I am offended by this.
“The Celtic people of Ireland and Great Britain also have high incidences of the RH- factor and it has recently been proven that there is a genetic link between the Basque and the Celts. This research proves that the Celtic people came from the Basque regions of France and Spain and a group must have migrated over to the islands of Great Britain.
As a direct result, Hemophilia became known as the “Royal Disease”. To keep this in perspective, only about 5% of all “royalty” have Rh-Factor negative blood…which means “less than the general population. That would indicate that the vast majority of “rulers” and “monarchs” are NOT Rhesus-factor negative. Is this by chance? or by genetic engineering called “arranged marriages”?
Is “hyper-creativity” a “symptom” of Rh-Negative Blood? Artists? Entertainers? Who knows…but if European Royalty refuse to marry into the Rh Negative blood line it means one thing…Rh-Neg people are a “competing royal line”.
It may be a method of DEPOPULATION beginning with infecting those GRADUALLY who are RH NEGATIVE.“
Self-reported vaccination for the current season was associated with a trend (P < 0.10) toward higher viral shedding in fine aerosol samples; vaccination with both the current and previous year’s seasonal vaccines, however, was significantly associated with greater fine-aerosol shedding in unadjusted and adjusted models (P < 0.01). In adjusted models, we observed 6.3 (95% CI 1.9–21.5) times more aerosol shedding among cases with vaccination in the current and previous season compared with having no vaccination in those two seasons.”
“The association of current and prior year vaccination with increased shedding of influenza A might lead one to speculate that certain types of prior immunity promote lung inflammation, airway closure, and aerosol generation. This first observation of the phenomenon needs confirmation. If confirmed, this observation, together with recent literature suggesting reduced protection with annual vaccination, would have implications for influenza vaccination recommendations and policies.”
“Prior immunity” promotes lung inflammation… Now I wanted to explain this part so that people wouldn’t be misled. Immunity and vaccination are not synonymous, in fact, this study provides the very evidence to prove that vaccinations like the influenza vaccine don’t provide immunity,
herd immunity is also a myth (search bar it)
hence the vaccinated being infected and spread it more. The correct wording should have read that “prior VACCINATIONS promote lung inflammation” as this fact has been shown in animal studies.
This means that when you receive a flu vaccine, elucidated by this study and animal studies, the lungs are damaged. Hence the scientific term/phrase “vaccine-associated enhanced respiratory disease” which in animal studies
has shown that flu vaccinations damage lung tissue of the vaccinated and distort or weaken the natural immunity of the host, person or animal. Could this be just one more reason more people are developing severe lung diseases like COPD or why the rates of asthma in America are increasing in the vaccinated?
The short and simple: The research shows…
The vaccine doesn’t protect one from infection.
That the vaccinated are “shedding”/spreading more virus simply by breathing.
That prior vaccination has weakened the immune systems of those who got the shot.
Individuals who receive the flu vaccine are placing others around them at greater risk than the unvaccinated.
In this article, we review the clinical management of deliberate infection with several pathogens of greatest bioweapons concern. On the basis of historical incidents coupled with information on ease of dissemination, contagiousness, mortality rates, public health impact, ability to engender panic, and the need for special preparedness,1-3 the Centers for Disease Control and Prevention (CDC) stratifies pathogens and toxins into three risk categories — A, B, and C — with category A meriting the highest level of concern and preparedness.4,5 In this review, we consider diseases that are caused by category A agents for which there are high-quality clinical data in the unclassified literature (see the Supplementary Appendix, available with the full text of this article at NEJM.org). The category A viral hemorrhagic fever viruses are beyond the scope of this review.
Pneumonic plague is caused by infection with the fleaborne bacteriumYersinia pestis. This organism, found worldwide and responsible for the “Black Death,” can cause several forms of illness: bubonic (the most common) (Figure 1D), septicemic, and pneumonic plague.41Because of the focus of this review, only pneumonic plague is discussed.
How fucking fascinating.
CARDINAL FEATURES OF PNEUMONIC PLAGUE
In a deliberate attack, primary pneumonic plague — rather than secondary spread from bubonic or septicemic forms — would occur 1 to 3 days after inhalation of the released bacterium or after droplet transmission from another infected person. The initial presentation of pneumonic plague is nonspecific and is difficult to differentiate from an ordinary pneumonia in its early stages. Hemoptysis, a unique feature, might be present, and rapid progression to respiratory failure and death would occur with greater frequency than in ordinary pneumonias.41
I imagine this would make the death count impossible to distinguish from regular pneumonia.
Remember: “Hemoptysis, a unique feature, might be present…”
“Maintaining that the 2019-nCoV may cause mild to severe respiratory disease, initially clinically presented as fever, dry cough, myalgia (muscle pain), fatigue and gradually progressing to a more severe productive cough that produces phlegm, episodic headaches, hemoptysis (coughing up blood) and occasional diarrhoea.”
What PP is versus what we’re told CV is by the MSM.
“Hemoptysis, a unique feature…”
Why has nobody else done it this way? aka the empirical one
look at signs, look at symptoms
u n i q u e f e a t u r e
I can’t be the only smartass.
But if I must.
DIAGNOSIS OF PNEUMONIC PLAGUE
Because the clinical features of pneumonic plague are nonspecific, diagnosis is largely based on the results of culture. Sputum, blood, or lymph-node aspirates could yield positive culture results. Chest radiography would reveal a severe pneumonic process. Serologic testing can also be useful but would not play much of a role during acute illness.41 Rapid antigen tests are available in regions in which plague is endemic, but none are FDA-approved.
So we’d see tests be useless early on…
and… a shortage of testing kits…
especially for America… who I imagine would call some state of emergency.
TREATMENT AND PREVENTION OF PNEUMONIC PLAGUE
The treatment of pneumonic plague involves a 10-day course of an aminoglycoside antibiotic agent, such as streptomycin or gentamicin. Doxycycline is considered a second-line treatment.41 However, a randomized, controlled trial of potential treatments for bubonic plague revealed equivalency between gentamicin and oral doxycycline; it is unclear whether these results can be extrapolated to pneumonic plague.42 There has been increased interest in the use of fluoroquinolones as primary treatment in mass-casualty settings.42 A 7-day course of doxycycline or ciprofloxacin would be used as postexposure prophylaxis.41No vaccine against plague is available. Because pneumonic plague can be transmitted from person to person through respiratory droplets, droplet precautions must be implemented for all patients.41
Why do the Chicoms want disease-ridden people in hospitals that can supposedly do nothing for them?
Yersinia pestis is the causative agent of plague, a zoonotic disease transmitted to humans through flea bites and typically characterized by the appearance of a tender and swollen lymph node, the bubo. Human-to-human transmission can occur, through either the bite of fleas (bubonic plague) or respiratory droplets, causing an overwhelming infection called pneumonic plague.
Our history books missed out that part.
Suddenly those masks don’t look so stupid.
The last plague pandemic began in Hong Kong in 1894 and spread throughout the world, establishing many endemic foci. Antibiotics and enforcement of public health measures significantly decreased the morbidity and mortality associated with the disease but did not allow its eradication. In fact, plague is now considered a reemerging disease1 ….
We report high-level resistance to multiple antibiotics, including all the drugs recommended for plague prophylaxis and therapy, in a clinical isolate of Y. pestis. The resistance genes were carried by a plasmid that could conjugate to other Y. pestis isolates. This report should serve as a warning of the risk of the spread of resistance in Y. pestis, a species previously considered universally susceptible to antibiotics.
…Strain 17/95 was resistant not only to all the antibiotics recommended for therapy (chloramphenicol, streptomycin, and tetracycline) and prophylaxis (sulfonamides and tetracycline) of plague4 but also to drugs that may represent alternatives to classic therapy, such as ampicillin, kanamycin, spectinomycin, and minocycline. The isolate remained susceptible to cephalosporins, other aminoglycosides, quinolones, and trimethoprim, and treatment with trimethoprim, despite its lack of synergism with sulfonamides, most likely led to the patient’s recovery….
The initial cases of novel coronavirus (2019-nCoV)–infected pneumonia (NCIP) occurred in Wuhan, Hubei Province, China, in December 2019 and January 2020. We analyzed data on the first 425 confirmed cases in Wuhan to determine the epidemiologic characteristics of NCIP.
identified by local hospitals using a surveillance mechanism for “pneumonia of unknown etiology” that was established in the wake of the 2003 severe acute respiratory syndrome (SARS) outbreak with the aim of allowing timely identification of novel pathogens such as 2019-nCoV.4 In recent days, infections have been identified in other Chinese cities and in more than a dozen countries around the world.5 Here, we provide an analysis of data on the first 425 laboratory-confirmed cases in Wuhan to describe the epidemiologic characteristics and transmission dynamics of NCIP.
Furthermore, children might be less likely to become infected or, if infected, may show milder symptoms, and either of these situations would account for underrepresentation in the confirmed case count. Serosurveys after the first wave of the epidemic would clarify this question.
re Pneumonic plague above: “Serologic testing can also be useful but would not play much of a role during acute illness.”
If it looks like a duck, walks like a duck and quacks like a duck – sure, it could be a chicken in a duck suit for kinky reasons but I’m inclined on probability to call it a fucking duck.
delays to hospitalization were much longer, with 89% of patients not being hospitalized until at least day 5 of illness (Figure 2). This indicates the difficulty in identifying and isolating cases at an earlier stage of disease.
re pneumonic plague, above: “The initial presentation of pneumonic plague is nonspecific and is difficult to differentiate from an ordinary pneumonia in its early stages.”
It’s the same hymn sheet. I can’t be the only one seeing this.
Our preliminary estimate of the incubation period distribution provides important evidence to support a 14-day medical observation period or quarantine for exposed persons.
re pneumonic plague, above: “In a deliberate attack, primary pneumonic plague — rather than secondary spread from bubonic or septicemic forms — would occur 1 to 3 days after inhalation of the released bacterium or after droplet transmission from another infected person.”
“The treatment of pneumonic plague involves a 10-day course of an aminoglycoside antibiotic agent, such as streptomycin or gentamicin. ”
“Because pneumonic plague can be transmitted from person to person through respiratory droplets, droplet precautions must be implemented for all patients.41“
That takes about…. 14 days.
Our study suffers from the usual limitations of initial investigations of infections with an emerging novel pathogen, particularly during the earliest phase, when little is known about any aspect of the outbreak and there is a lack of diagnostic reagents.
re pneumonic plague: “The initial presentation of pneumonic plague is nonspecific and is difficult to differentiate from an ordinary pneumonia in its early stages.”
re pneumonic plague: “diagnosis is largely based on the results of culture”
Furthermore, the initial focus of case detection was on patients with pneumonia, but we now understand that some patients can present with gastrointestinal symptoms, and an asymptomatic infection in a child has also been reported.17
“Pneumonic plague: Patients develop fever, headache, weakness, and a rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery mucous. Pneumonic plague may develop from inhaling infectious droplets or may develop from untreated bubonic or septicemic plague after the bacteria spread to the lungs. The pneumonia may cause respiratory failure and shock. Pneumonic plague is the most serious form of the disease and is the only form of plague that can be spread from person to person (by infectious droplets).”
“Pneumonic plague affects the lungs. It’s the least common variety of plague but the most dangerous, because it can be spread from person to person via cough droplets. Signs and symptoms can begin within a few hours after infection, and may include:
Cough, with bloody mucus (sputum)
Nausea and vomiting
Pneumonic plague progresses rapidly and may cause respiratory failure and shock within two days of infection. Pneumonic plague needs to be treated with antibiotics within a day after signs and symptoms first appear, or the infection is likely to be fatal.”
repeating coronavirus paper:
Although delays between the onset of illness and seeking medical attention were generally short, with 27% of patients seeking attention within 2 days after onset.
Back to CV paper generally
Early infections with atypical presentations may have been missed, and it is likely that infections of mild clinical severity have been under-ascertained among the confirmed cases.18 We did not have detailed information on disease severity for inclusion in this analysis.
In conclusion, we found that cases of NCIP have been doubling in size approximately every 7.4 days in Wuhan at this stage. Human-to-human transmission among close contacts has occurred since the middle of December and spread out gradually within a month after that. Urgent next steps include identifying the most effective control measures to reduce transmission in the community. The working case definitions may need to be refined as more is learned about the epidemiologic characteristics and outbreak dynamics. The characteristics of cases should continue to be monitored to identify any changes in epidemiology — for example, increases in infections among persons in younger age groups or health care workers. Future studies could include forecasts of the epidemic dynamics and special studies of person-to-person transmission in households or other locations, and serosurveys to determine the incidence of the subclinical infections would be valuable.14
re Pneumonic plague above: “Serologic testing can also be useful but would not play much of a role during acute illness.”
These initial inferences have been made on a “line list” that includes detailed individual information on each confirmed case, but there may soon be too many cases to sustain this approach to surveillance, and other approaches may be required.19
Study allowed by Chinese Government, who arrested 8 doctors for trying to release some piece of information, can’t imagine what.
If they’d been told to give people antibiotics for a virus though, I imagine they had some pointed questions.
Especially if the Chicoms wanted to buy time to buy up global supply and produce more.
“Pneumonic plague is a severe lung infection caused by the bacterium Yersinia pestis. Symptoms include fever, headache, shortness of breath, chest pain, and cough. They typically start about three to seven days after exposure.”
Long lag time.
PP can cause meningitis, which might explain the headache.
from CV article above: “”Common coronavirus symptoms can include: — Fever — Dry cough — Shortness of breath — Aching muscles — Fatigue”
“For confirmed 2019-nCoV infections, reported illnesses have ranged from people with little to no symptoms to people being severely ill and dying. Symptoms can include:
Shortness of breath”
All three just so happen to be also the symptoms of pneumonic plague.
“CDC believes at this time that symptoms of 2019-nCoV may appear in as few as 2 days or as long as 14 after exposure”
So three, three days on the low end. How familiar.
About dat headache symptom…
Coronaviruses as Encephalitis
-Inducing Infectious Agents
so why is headache not described as a symptom?
“In acute encephalitis, viral replication occurs in the brain tissue itself, possibly causing destructive lesions of the gray matter, as was described after herpes simplex virus (HSV), rabies, or some arbovirus infections. ”
Yes, herpes can reach the brain. Again, I must remind you. Yes, it can.
This concludes why I’m banned from appearing on tv (pretty much).
A comparison between eight individual samples demonstrated that the Asian male one has an extremely large number of ACE2-expressing cells in the lung. This study provides a biological background for the epidemic investigation of the 2019-nCov infection disease, and could be informative for future anti-ACE2 therapeutic strategy development.
We may dub it The Elliot gene.
…..We also noticed that the only Asian donor (male) has a much higher ACE2-expressing cell ratio than white and African American donors (2.50% vs. 0.47% of all cells). This might explain the observation that the new Coronavirus pandemic and previous SARS-Cov pandemic are concentrated in the Asian area….
Almost like the Chinese wanted to wipe out most of their own race IF there were a war.