16-Year-Old Girl Trusted Science Instead of Her Parents and Got Vaxed; Now Has Neurological Problems

Snake Baker

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I wonder if she still LOVES SCIENCE!!!

Is it maybe possible to love science so hard that it hurts?

Children’s Health Defense:

Sarah Green was a healthy 16-year-old — until she developed neurological problems after getting Pfizer’s COVID vaccine. But doctors said her new tremors, tics and debilitating migraines couldn’t possibly be caused by the vaccine.

In an exclusive interview with The Defender, Sarah and her mother, Marie Green, said they feel helpless because nobody will acknowledge Sarah’s vaccine injury and “nobody can help them.”

Sarah received her second dose of Pfizer on May 4, and immediately experienced a headache at the base of her neck that radiated to her temples. She said it felt like she got “‘hit by a bus.” She took a nap in hopes she could sleep it off.

The headaches never went away and slowly, over the course of three weeks, Sarah developed small facial twitches.

“The night of May 23, I went to my dad because my neck had started twitching every 15 seconds,”
Sarah said.

Green said Sarah would start a word and it was as if her brain would reset. “It wasn’t like she was trying to get a word out — it would just start over.”

After Sarah’s symptoms worsened, her parents took her to Johnston Health in Smithfield, North Carolina. Upon arrival the physicians noticed Sarah had constant tremors. Green said the doctor looked down and noticed Sarah’s right foot also had a tremor, but they didn’t have a pediatric neurologist, so she was transferred to WakeMed in Raleigh once she stabilized.

Sarah’s EEG, MRI with and without contrast and CT scans were normal. After two days the doctor came in and said Sarah had a nervous twitch and needed to see a mental health professional.

During the MRI with contrast, Sarah’s mother said she stopped breathing and had to be pulled out of the machine and intubated. Two hours later the doctor came in and said they were going to send Sarah home.

“They weren’t even going to refer her to a neurologist,”
Green said. “They said it was just a nervous tick and she needed to see a therapist.”

Green said the vaccine was not the first thing she thought of when her daughter’s symptoms initially started, but the hospital had her fill out a form of things that might have changed and “when it came down to it, the only thing that changed was the vaccine.”

When Green asked the doctor if the vaccine could have caused her daughter’s condition, he got very defensive and said, “We can’t blame everything on the vaccine.”

Green said the physician’s response was frustrating. “How can you say you don’t know what it is but say the vaccine isn’t the cause?” she asked.

Green said, “As soon as we said it was the vaccine, it was like they couldn’t get us out of there fast enough.”

When Sarah finally got into a neurologist on June 6, Green asked if Sarah’s condition was vaccine-related.

The doctor said Sarah had functional movement disorder and it was not related to the vaccine — although she said she has seen more cases since COVID vaccines were approved because people “stress themselves out over the vaccine and it’s psychosomatic.”


According to the National Organization of Rare Disorders, functional movement disorder is a type of functional neurological disorder that occurs when there is a problem with the functioning of the nervous system and how the brain and body send and/or receive signals — rather than a structural disease process, such as multiple sclerosis or stroke.

The condition can encompass a wide variety of neurological symptoms, such as tremors, dystonia, jerky movements (myoclonus) and problems walking (gait disorder).

Green didn’t agree with the doctor’s assessment that Sarah’s reaction was “psychosomatic.”

“Sarah is 16. She was nervous about getting a needle in her arm, but once she got the vaccine she slapped a bandaid on it and went off to starbucks,” Green said.

“When I tried to explain that to her neurologist, she said that I needed to stop focusing on what caused it and focus on getting my daughter well,” Green explained. “But I felt like if we didn’t know why, we wouldn’t be able to treat her the right way.”

Green said Sarah got the vaccine on her own because in North Carolina, she could get the vaccine without parental consent.

“She works in fast food and on the frontline and they were told the vaccine would be mandated,” Green said. “Krispy Kreme was giving out a dozen donuts, so the kids went and got their shots.”

Green said neither she nor her husband got a COVID vaccine. When Sarah said she wanted to get it, Green explained her and her husband’s reservations and why they weren’t getting the vaccine.

Green said:

“We have been asked many times why she got it and we didn’t. She did come to us and tell us she wanted to, but we did not know she had made up her mind. We had a discussion about it, but her job and the free incentives that I feel were targeted towards young people — Krispy Kreme offered them a dozen free donuts — really swayed her decision.

Sarah was told the risks of getting a vaccine included having a sore arm for a few days, but now it has been months and she’s not fine.


Sarah had to drop two college classes this semester because of her symptoms. “She had just started driving but she cannot drive anymore because she can’t look up or turn her head to the right without it causing spastic tremors. She also can’t write,” Green said. “She has constant tremors like someone who has Parkinson’s disease.”

Sarah’s symptoms have progressively worsened over time, but the only treatment option recommended to her was a medication similar to Benadryl.

Green said:

“It’s so frustrating. We tried to get her into a hospital in Florida but there is a six-month waiting list. We called Cleveland but they have a three-month waiting list. We have called the Shriners hospital and they won’t even see her. We had an appointment at Duke but it was going to be on a video conference. We just keep getting doors slammed in our faces and the minute you mention a vaccine they don’t want to deal with you anymore.”



Green said she reported Sarah’s vaccine injury to the Centers for Disease Control and Prevention’s (CDC) Vaccine Adverse Event Reporting System (I.D. 1354500) and Pfizer.

“When I called Pfizer they just had me answer some questions and said if there were new symptoms to call back and they could update their report,” Green said. “When I called back a second time they said they lost the report. When I asked if anyone else had called with the same symptoms they said ‘no.’”
The most interesting thing that I found about this story is that when a woman has brain damage they get the same look on their face they get when they’re having sex.



Not a day goes by that I don’t feel strong jealousy for the incels who have never seen that look on a woman’s face, while you are on top of her, filled with such extreme disgust and self-loathing.

I guess for a woman, having brain damage is like having a permanent orgasm.

No wonder they’re so excited about getting this vaccine.

People you to say to me, “you just hate women.”

And I would be like “I don’t hate women, but…”

Now, I just say “that’s correct.”

Elliot Rodger was right.

You know who else was right?

RFK Jr.

Dominique is still searching for answers from doctors after developing a long list of debilitating conditions, including severe neurological complications, pain and at times, an inability to walk, following her first dose of Pfizer’s COVID vaccine.https://t.co/pl06mjTjdP

— Robert F. Kennedy Jr (@RobertKennedyJr) September 9, 2021

The lucky thing for big pharma is that because they spend so much money paying off politicians, the politicians made it so they can’t be sued.

What incentive do they have to not hurt you when they can’t be sued?

If you add in the fact that the government will force you to use their products, they don’t even have to worry about you finding out that these vaxes are killing and maiming people. You can find out about that, but if you talk about it you will be silenced, and if you don’t take the shot you will be fired and banned from everything.

This is such just a really dumb tyranny.

I think the problem is that people are so fat, they have all this fat in their brains, and they just can’t even think.

Continue reading...
 

Yang Wen-Li

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Krispy Kreme got paid by the vax companies to give out the donuts, or the government. Don‘t kid yourselves they did it for free.
Anyway, this is the fault of the unvaxed.
I wouldn't be so sure. It's certainly possible but I can see them doing if of their own volition too.
 

Louisa_Reese

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So glad vaccinated teens are considered weird in my 16 year old's peer group. Or at the very least they are considered "under the thumb of his mom."

Peer pressure at that age is real and if all your friends are getting the vax they will think something is wrong with you if you're not. But it goes both ways - if none of your friends are getting the vax they will think something is wrong with you if you're the only one to get it (at least if you get it voluntarily).
 

Freedom Monk

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I know I'm supposed to feel bad for those of us of the lesser intellectual disposition to see reality (woman), but boy oh boy the physiognomy on that girl just screams out to me "permanent AWFL", especially with the smarmy look on its face, the slight pursing of the lips and the iconic "problem glasses". Thats the look of a woman who would get a dopamine hit in the brain from seeing big daddy authoritative government torturing an anti-vaxx dissident to death after she rats him out to them.

What did the man in funny clown makeup shout out to the tv presenter before he shot him again?

“Sarah is 16. She was nervous about getting a needle in her arm, but once she got the vaccine she slapped a bandaid on it and went off to starbucks,” Green said.
The memes write themselves, need I say more?
 

Aryan Uprising

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I think the problem is that people are so fat, they have all this fat in their brains, and they just can’t even think.
Hey, I think you'z being a bit hard extremist here. The poor wee lassie may hav become a brain-damaged spastic, but... hav u ever tasted crispy creme donuts? Mmmmmmmmm
 

anti-barabas-ite

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On a deadlier note, a fat black 19 year old kid of EXNFL player died mysterious recently.

If they dont tell you right off it's a negro in the story....its a negro.

Im expanding that rule, if they are young, Die mysterious like...its sarscov2aids vax death!
 

Im the horse

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I know I'm supposed to feel bad for those of us of the lesser intellectual disposition to see reality (woman), but boy oh boy the physiognomy on that girl just screams out to me "permanent AWFL", especially with the smarmy look on its face, the slight pursing of the lips and the iconic "problem glasses". Thats the look of a woman who would get a dopamine hit in the brain from seeing big daddy authoritative government torturing an anti-vaxx dissident to death after she rats him out to them.

What did the man in funny clown makeup shout out to the tv presenter before he shot him again?



The memes write themselves, need I say more?
These were my exact thoughts. Every word you said. 100% accurate.
 

Herminator

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Guys look angry when they're banging and women look like they're being hurt, it's a good match if you ask me.
Wow. That is very true and interesting. When I had a porn problem I also noticed that women look like they are in terrible pain, this is even more noticeable with the sound off.
 

AlbertStokes

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So glad vaccinated teens are considered weird in my 16 year old's peer group. Or at the very least they are considered "under the thumb of his mom."

Peer pressure at that age is real and if all your friends are getting the vax they will think something is wrong with you if you're not. But it goes both ways - if none of your friends are getting the vax they will think something is wrong with you if you're the only one to get it (at least if you get it voluntarily).
Heaps are getting vaxed in the Sydney area and outside of the area in Australia. My daughter can't play sport and lost her little job because she isn't vaxxed. All of her associates are vaxxed or getting it, no questions asked. She is home schooled.
 

CrackSmokeRepublican

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Wow. That is very true and interesting. When I had a porn problem I also noticed that women look like they are in terrible pain, this is even more noticeable with the sound off.
Yeah...they are being "invaded"...from personal observation...they like it most when they can't control it. Seen it.
 

CrackSmokeRepublican

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Protection of White Wombs is paramount at this point. Covid-19 Vaxxed or infected seems to have a limited effect fortunately. Get them pregnant young and able before infection is my advice:

COVID-19 can be transmitted in the womb, reports pediatric infectious disease journal
]Case study provides evidence of intrauterine transmission of SARS-CoV-2 from mother to infant
Date: July 10, 2020 Source: Wolters Kluwer Health Summary:
A baby girl in Texas -- born prematurely to a mother with COVID-19 -- is the strongest evidence to date that intrauterine (in the womb) transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can occur, according to a new report.


Note that this dude tries to debunk the above:


Article on Covid-19 (Vaxx or simply infected with Covid-19):

Diagnostics (Basel). 2021 Jan; 11(1): 94.
Published online 2021 Jan 8. doi: 10.3390/diagnostics11010094
PMCID: PMC7827584
PMID: 33435547
The Effects of COVID-19 on Placenta and Pregnancy: What Do We Know So Far?
Yin Ping Wong,1,* Teck Yee Khong,2 and Geok Chin Tan1,*
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.

Associated Data
Supplementary MaterialsData Availability Statement
Go to:

Abstract
The current coronavirus disease 2019 (COVID-19) pandemic, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has inflicted a serious health crisis globally. This virus is associated with a spectrum of respiratory illness ranging from asymptomatic, mild to severe pneumonia, and acute respiratory distress syndrome. Accumulating evidence supports that COVID-19 is not merely a respiratory illness per se, but potentially affects other organ systems including the placenta. SARS-CoV-2 gains access to human cells via angiotensin-converting enzyme 2 (ACE-2). The abundance of ACE-2 on the placental cell surface, especially the syncytiotrophoblasts, could potentially contribute to vertical transplacental transmission to the fetus following maternal COVID-19 infection. Intriguingly, despite the placentas being tested positive for SARS-CoV-2, there are very few newborns that manifest virus-induced diseases. The protective effects of the placental barrier to viral infection, limiting the spread of the virus to newborn infants, remain a mystery. The detrimental role of COVID-19 in pregnancies is largely debatable, although COVID-19 maternal infection has been implicated in unfavorable pregnancy outcomes. In this review, we summarize the pathological features manifested in placenta due to COVID-19 maternal infection that have been previously reported, and relate them to the possible disease manifestation. The potential mechanistic pathways associated with transplacental viral transmission and adverse pregnancy outcomes are also discussed.
Keywords: COVID-19, pathology, placenta, pregnancy, SARS-CoV-2
Go to:
1. Introduction
The 2019 coronavirus disease (COVID-19), a novel zoonotic disease [1], was first discovered in late December 2019 following an outbreak of severe pneumonia of unknown etiology in Wuhan, Hubei Province, China. The etiological agent was successfully isolated and identified as a previously unknown beta-coronavirus, which was provisionally coined as 2019 novel coronavirus (2019-nCoV) [2]. It was later officially designated as Severe Acute Respiratory Syndrome Virus 2 (SARS-CoV-2) on the ground of phylogenetic analysis by the International Committee on Taxonomy of Viruses [3]. The emergence and rapid spread of SARS-CoV-2 via sustained human-to-human transmission poses a formidable pandemic threat to humankind globally. COVID-19 was declared as the fifth documented pandemic on 11 March 2020 by the World Health Organization (WHO) after the 2009 Influenza A (H1N1) swine flu [4]. As of 9 November 2020, there were estimated to be 50.4 million confirmed cases worldwide with 1.26 million deaths, accounting for an almost 2.5% death rate [5].
SARS-CoV-2 infection has taken healthcare providers by surprise, as it behaves like no other “respiratory” infection, and lungs are not the only organs being affected. A proportion of patients with severe COVID-19 presented with extrapulmonary clinical manifestations related to cardiac-, kidney-, liver-, digestive tract-injuries, and neurological disorders [6], besides suffering from classic respiratory symptoms and fever. Placentas are no exception. There is increasing evidence that COVID-19 infection leaves tell-tale signs of injuries in the placenta.
Interestingly, despite the increasing molecular and ultrastructural evidence of SARS-CoV-2 in the placentas of COVID-19-positive mothers, newborns have yet to manifest virus-induced diseases [7]. No teratogenic effect of COVID-19 infection in the neonate has been reported. Gajbhiye et al. (2020) observed that only 24 (8%) out of 313 neonates born to mothers with COVID-19 tested positive for SARS-CoV-2 [8], which raises an important question on the success rate of transplacental viral infection (intrauterine transmission) to the fetus. Noteworthy, maternal infection does not equate to placental infection. Likewise, evidence of placental viral infection does not guarantee intrauterine vertical transmission to fetus [9]. It is assumed that there will be an active replication of the virus in the placenta. However, if this is true, the mechanism involved in preventing this highly infectious virus from reaching the fetus is still unclear. Possibilities include the maternal–fetal interface of placenta acting as a strong barrier against infection, or the absence of specific pathways/receptors that allow effective viral transmission.
The human placenta has an immunological barrier to the entry of pathogens, besides maintaining immune tolerance to the fetal cells. The key role of innate immune system in protecting the fetuses and neonates against SARS-CoV-2 infection has been proposed [10]. Decidua basalis, being the maternal component of the maternofetal interface, contains diverse immune cells that belong to the innate immune system including natural killer (NK) cells (70%), decidual macrophages (15%), and CD4 T cells (15%) [11]. In addition, the syncytiotrophoblast cells, outermost layer of chorionic villi, which are in direct contact with the maternal blood, do not contain an intercellular gap junction, and thus prevent entry of pathogens from the maternal blood. Physical obstacles including trophoblastic basement membranes create an additional physical barrier against pathogens [9]. Taken together, the innate immune system, structural barrier, as well as the interaction between decidual immune cells and the invading fetal extravillous trophoblasts may play a role in the placental protective mechanisms against SARS-CoV-2 viral invasion.
Unequivocal diagnosis of SARS-CoV-2 transplacental infection requires the detection of viral RNAs in placenta, amniotic fluid prior to the onset of labor, cord or neonatal blood/body fluid/respiratory samples, or demonstration of viral particles by electron microscopy, immunohistochemistry, or in situ hybridization method in fetal/placental tissues [12]. The usefulness of serological testing in the diagnosis of SARS-CoV-2 infection is yet to be confirmed [13]. The specificity of IgM testing is questionable, due to high false positivity [14]. Alternatively, testing for viral load in both the maternal and fetal plasma (viraemia) in lieu of nasopharyngeal swab may be useful to determine if the risk of transmission positively correlated with maternal viral load, besides helping to estimate the transmission rate more accurately.
Placental examination can yield invaluable information that may be essential to enhance our understanding of disease pathogenesis and to identify underlying causes of adverse pregnancy outcomes [15]. Due to the novelty of COVID-19, histomorphological and ultrastructural changes reported on placentas from SARS-CoV-2-positive women are limited to isolated case reports and a handful of case series. The knowledge gap between the effects of COVID-19 on placenta and pregnancy outcomes needs to be explored.
With the aim to address this issue, we performed a literature search on the MEDLINE/PubMed electronic database using keywords “COVID-19”, “SARS-CoV-2”, and “placenta”. Reference lists of the included papers were also checked to identify additional relevant studies. We reviewed all articles (both peer-reviewed and preprints) with reports on placental pathology in pregnant women tested positive for SARS-CoV-2 that were published between 1 January 2020 to 10 October 2020 (n = 29) [16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44]. Articles written in languages other than English and Mandarin were excluded. Clinical characteristics of the SARS-CoV-2 included studies were summarized in Table S1.
Go to:
2. SARS-CoV-2 and Pregnancy
Coronaviruses (CoV) including Severe Acute Respiratory Syndrome (SARS)-Co-V, Middle East Respiratory Syndrome (MERS)-CoV, hCoV-HKU1, and hCoV-OC43 are among the known zoonotic viruses that cause respiratory and gastrointestinal infections in humans [45], with SARS-CoV-2 being the latest discovered. SARS-CoV-2, like its predecessors SARS-CoV and MERS-CoV, is highly pathogenic and lethal, causing severe pneumonia, acute respiratory distress syndrome (ARDS), multi-organ failure, and death [46].
SARS-CoV-2 is a large, spherical, enveloped, single stranded positive-sense ribonucleic acid (RNA) virus with genome size approximately 30 kilobase (kb) in length. There are four major structural proteins that form the backbone of the virus: The spike (S) protein, membrane (M) protein, envelope (E) protein, and nucleocapsid (N) protein. The unique structural protein, the spike (S) protein, which is present in abundance on the viral cell surface, plays a key role in its pathogenesis [47].
Pregnancy has always been associated with an increased risk of acquiring respiratory infection with higher morbidity and mortality than the nonpregnant subjects [48]. In a systematic review examining 2567 COVID-19 confirmed pregnancies with 746 deliveries, there were 3.4% women with maternal critical disease requiring mechanical ventilation support, 0.9% maternal death, and 21.8% preterm birth, primarily iatrogenic rather than spontaneous, and less than 1% perinatal death [49]. In another systematic review on 324 pregnancies with COVID-19, it was reported that up to 14% mothers with severe pneumonia required critical care, with a total of 9 cases of maternal deaths, 4 cases of spontaneous abortion, 4 cases of intrauterine fetal deaths, and 3 cases of neonatal death [50]. Brandt et al. (2020) conducted a matched case-control study involving 61 COVID-19 pregnancies matched to 2 controls by delivery date, and reported that the odds of adverse composite outcomes for mother and fetus were 3.4 times and 1.7 times higher among severe/critical COVID-19 cases than controls, respectively, with maternal advance age, obesity, Hispanic or Latino origin, and other medical comorbidities being some of the important factors driving a more severe clinical course. Reassuringly, pregnant women who were asymptomatic or had mild COVID-19 disease were observed to have benign outcomes [51].
The anatomical and physiological changes of the respiratory system as well as immunological and hormonal adaptation during pregnancy collectively make them more vulnerable to certain infections, including SARS-CoV-2 [52,53]. Anatomical and physiological changes in the maternal respiratory system include relaxation of rib ligaments, diaphragmatic elevation, and reduction in the functional residual capacity (FRC) of the lung initiated by the effects of progesterone, and hence ineffective airway clearance [53]. Functional ventilation and perfusion mismatch as a sequela of reduced FRC also increases the severity of respiratory infection. Besides, immunological modulation by a physiological shift to Th2 dominant environment and attenuation of Th1 cell-mediated immunity during pregnancy has increased viral infection risks. It does not only affect the viral clearance rate, but hastens the disease deterioration [54].
Notably, SARS-CoV-2 infects target host cells by binding to the cell membrane angiotensin-converting enzyme II (ACE2), facilitated by S protein priming proteases Type II transmembrane serine protease (TMPRSS2). ACE2 is a membrane-bound aminopeptidase enzyme that has a physiological role in degrading substances including angiotensins I and II, a key protective mechanism in regulating vascular and heart functions. It is found in most organs such as heart, lung, kidney, vessels, brain, and others, including the placenta [55]. The types of cell in placenta that express ACE2 are the syncytiotrophoblasts and cytotrophoblasts in villi, decidual stromal cells, decidual perivascular cells, and endothelial and vascular smooth muscle cells. The co-expression of the viral receptor ACE2 and TMPRSS2 in abundance in the human placenta theoretically may increase vulnerability of placenta and possibly fetus to SARS-CoV-2 infection [56,57].
Interestingly, subsequent studies pursued by Bloise et al. (2020) revealed that ACE2 and TMPRSS2 were differentially expressed at different stages of pregnancy. They observed that ACE2 and TMPRSS2 expressions in placenta were negatively correlated with gestational age, in which their expression levels in reducing trend from first trimester to second trimester placenta, and very low to almost undetectable in third trimester preterm and term placenta [57]. The authors concluded that the first trimester of pregnancy was possibly more vulnerable to SARS-CoV-2 transplacental transmission than in later stages of pregnancy [57]. Surprisingly, SARS-CoV-2 was not detected in the abortus/placenta in the few reported cases of first and second trimester miscarriages despite the mothers being tested positive for COVID-19 [19,58], but was found to be positive in amniotic fluid and infant born pre-term to a COVID-19-positive mother in the third trimester [59], even though, theoretically, third trimester infants should be protected from acquiring COVID-19 infection since there is a paucity of the required receptors present in the placenta.
In addition, Kotlyar et al. (2019), in their systematic review revealed that SARS-CoV-2 positivity detection rate from neonatal nasopharyngeal swab, cord blood, placenta samples, amniotic fluid, and serology was extant although low (ranges from 0–7.7%) [60]. It is possible that there is another alternate entry of SARS-CoV-2 into placenta cells beyond ACE2. Alternatively, it is possible that the presence of underdiagnosed/asymptomatic concurrent genital tract infection breaches the placental barrier and allows entry of the virus into amniotic cavity.
Viraemia is a prerequisite for transplacental transmission to occur. Emerging evidence showed that plasma viral load in COVID-19 cases was positively correlated with the disease severity [61]. Infants born to mothers with severe to critical COVID-19 diseases showed higher rates of SARS-CoV-2 positivity detected in the placenta and nasopharyngeal swab immediately after birth [26,62], supporting the viraemia hypothesis. Overall prevalence of viraemia in COVID-19 infected individuals, however, is low and transient [63], which makes placental seeding rather impossible and hence, the low rate of transplacental transmission. Arguably, the mere detection of viral RNA in the blood/serum does not reflect infectivity of a virus. Andersson et al. (2020) found that all their reverse transcription-polymerase chain reaction (RT-PCR)-positive clinical samples show neither viral replication nor display any cytopathic effect after inoculation in cell culture [64]. More studies are warranted to resolve these uncertainties.


This too:
https://dadamo.com/dangerous/2020/04/04/covid-19-ace2/ (how the body creates energy for growth is via ACE2 receptors which covid and covid vaxxes short-circuits.)
 

anti-barabas-ite

Work stuff through in your brain...UNVAXXED
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On a deadlier note, a fat black 19 year old kid of EXNFL player died mysterious recently.

If they dont tell you right off it's a negro in the story....its a negro.

Im expanding that rule, if they are young, Die mysterious like...its sarscov2aids vax death!
keshawn johnsons 22 year old daughter mysteriously died this year too...

google allowed stories read almost exactly the same, when they get shot they tell you, if its a vag cancer they tell you, if its a vac induced suicide they won't say.
 

anti-barabas-ite

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Protection of White Wombs is paramount at this point. Covid-19 Vaxxed or infected seems to have a limited effect fortunately. Get them pregnant young and able before infection is my advice:

COVID-19 can be transmitted in the womb, reports pediatric infectious disease journal
]Case study provides evidence of intrauterine transmission of SARS-CoV-2 from mother to infant
Date: July 10, 2020 Source: Wolters Kluwer Health Summary:
A baby girl in Texas -- born prematurely to a mother with COVID-19 -- is the strongest evidence to date that intrauterine (in the womb) transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can occur, according to a new report.


Note that this dude tries to debunk the above:


Article on Covid-19 (Vaxx or simply infected with Covid-19):

Diagnostics (Basel). 2021 Jan; 11(1): 94.
Published online 2021 Jan 8. doi: 10.3390/diagnostics11010094
PMCID: PMC7827584
PMID: 33435547
The Effects of COVID-19 on Placenta and Pregnancy: What Do We Know So Far?
Yin Ping Wong,1,* Teck Yee Khong,2 and Geok Chin Tan1,*
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.

Associated Data
Supplementary MaterialsData Availability Statement
Go to:

Abstract
The current coronavirus disease 2019 (COVID-19) pandemic, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has inflicted a serious health crisis globally. This virus is associated with a spectrum of respiratory illness ranging from asymptomatic, mild to severe pneumonia, and acute respiratory distress syndrome. Accumulating evidence supports that COVID-19 is not merely a respiratory illness per se, but potentially affects other organ systems including the placenta. SARS-CoV-2 gains access to human cells via angiotensin-converting enzyme 2 (ACE-2). The abundance of ACE-2 on the placental cell surface, especially the syncytiotrophoblasts, could potentially contribute to vertical transplacental transmission to the fetus following maternal COVID-19 infection. Intriguingly, despite the placentas being tested positive for SARS-CoV-2, there are very few newborns that manifest virus-induced diseases. The protective effects of the placental barrier to viral infection, limiting the spread of the virus to newborn infants, remain a mystery. The detrimental role of COVID-19 in pregnancies is largely debatable, although COVID-19 maternal infection has been implicated in unfavorable pregnancy outcomes. In this review, we summarize the pathological features manifested in placenta due to COVID-19 maternal infection that have been previously reported, and relate them to the possible disease manifestation. The potential mechanistic pathways associated with transplacental viral transmission and adverse pregnancy outcomes are also discussed.
Keywords: COVID-19, pathology, placenta, pregnancy, SARS-CoV-2
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1. Introduction
The 2019 coronavirus disease (COVID-19), a novel zoonotic disease [1], was first discovered in late December 2019 following an outbreak of severe pneumonia of unknown etiology in Wuhan, Hubei Province, China. The etiological agent was successfully isolated and identified as a previously unknown beta-coronavirus, which was provisionally coined as 2019 novel coronavirus (2019-nCoV) [2]. It was later officially designated as Severe Acute Respiratory Syndrome Virus 2 (SARS-CoV-2) on the ground of phylogenetic analysis by the International Committee on Taxonomy of Viruses [3]. The emergence and rapid spread of SARS-CoV-2 via sustained human-to-human transmission poses a formidable pandemic threat to humankind globally. COVID-19 was declared as the fifth documented pandemic on 11 March 2020 by the World Health Organization (WHO) after the 2009 Influenza A (H1N1) swine flu [4]. As of 9 November 2020, there were estimated to be 50.4 million confirmed cases worldwide with 1.26 million deaths, accounting for an almost 2.5% death rate [5].
SARS-CoV-2 infection has taken healthcare providers by surprise, as it behaves like no other “respiratory” infection, and lungs are not the only organs being affected. A proportion of patients with severe COVID-19 presented with extrapulmonary clinical manifestations related to cardiac-, kidney-, liver-, digestive tract-injuries, and neurological disorders [6], besides suffering from classic respiratory symptoms and fever. Placentas are no exception. There is increasing evidence that COVID-19 infection leaves tell-tale signs of injuries in the placenta.
Interestingly, despite the increasing molecular and ultrastructural evidence of SARS-CoV-2 in the placentas of COVID-19-positive mothers, newborns have yet to manifest virus-induced diseases [7]. No teratogenic effect of COVID-19 infection in the neonate has been reported. Gajbhiye et al. (2020) observed that only 24 (8%) out of 313 neonates born to mothers with COVID-19 tested positive for SARS-CoV-2 [8], which raises an important question on the success rate of transplacental viral infection (intrauterine transmission) to the fetus. Noteworthy, maternal infection does not equate to placental infection. Likewise, evidence of placental viral infection does not guarantee intrauterine vertical transmission to fetus [9]. It is assumed that there will be an active replication of the virus in the placenta. However, if this is true, the mechanism involved in preventing this highly infectious virus from reaching the fetus is still unclear. Possibilities include the maternal–fetal interface of placenta acting as a strong barrier against infection, or the absence of specific pathways/receptors that allow effective viral transmission.
The human placenta has an immunological barrier to the entry of pathogens, besides maintaining immune tolerance to the fetal cells. The key role of innate immune system in protecting the fetuses and neonates against SARS-CoV-2 infection has been proposed [10]. Decidua basalis, being the maternal component of the maternofetal interface, contains diverse immune cells that belong to the innate immune system including natural killer (NK) cells (70%), decidual macrophages (15%), and CD4 T cells (15%) [11]. In addition, the syncytiotrophoblast cells, outermost layer of chorionic villi, which are in direct contact with the maternal blood, do not contain an intercellular gap junction, and thus prevent entry of pathogens from the maternal blood. Physical obstacles including trophoblastic basement membranes create an additional physical barrier against pathogens [9]. Taken together, the innate immune system, structural barrier, as well as the interaction between decidual immune cells and the invading fetal extravillous trophoblasts may play a role in the placental protective mechanisms against SARS-CoV-2 viral invasion.
Unequivocal diagnosis of SARS-CoV-2 transplacental infection requires the detection of viral RNAs in placenta, amniotic fluid prior to the onset of labor, cord or neonatal blood/body fluid/respiratory samples, or demonstration of viral particles by electron microscopy, immunohistochemistry, or in situ hybridization method in fetal/placental tissues [12]. The usefulness of serological testing in the diagnosis of SARS-CoV-2 infection is yet to be confirmed [13]. The specificity of IgM testing is questionable, due to high false positivity [14]. Alternatively, testing for viral load in both the maternal and fetal plasma (viraemia) in lieu of nasopharyngeal swab may be useful to determine if the risk of transmission positively correlated with maternal viral load, besides helping to estimate the transmission rate more accurately.
Placental examination can yield invaluable information that may be essential to enhance our understanding of disease pathogenesis and to identify underlying causes of adverse pregnancy outcomes [15]. Due to the novelty of COVID-19, histomorphological and ultrastructural changes reported on placentas from SARS-CoV-2-positive women are limited to isolated case reports and a handful of case series. The knowledge gap between the effects of COVID-19 on placenta and pregnancy outcomes needs to be explored.
With the aim to address this issue, we performed a literature search on the MEDLINE/PubMed electronic database using keywords “COVID-19”, “SARS-CoV-2”, and “placenta”. Reference lists of the included papers were also checked to identify additional relevant studies. We reviewed all articles (both peer-reviewed and preprints) with reports on placental pathology in pregnant women tested positive for SARS-CoV-2 that were published between 1 January 2020 to 10 October 2020 (n = 29) [16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44]. Articles written in languages other than English and Mandarin were excluded. Clinical characteristics of the SARS-CoV-2 included studies were summarized in Table S1.
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2. SARS-CoV-2 and Pregnancy
Coronaviruses (CoV) including Severe Acute Respiratory Syndrome (SARS)-Co-V, Middle East Respiratory Syndrome (MERS)-CoV, hCoV-HKU1, and hCoV-OC43 are among the known zoonotic viruses that cause respiratory and gastrointestinal infections in humans [45], with SARS-CoV-2 being the latest discovered. SARS-CoV-2, like its predecessors SARS-CoV and MERS-CoV, is highly pathogenic and lethal, causing severe pneumonia, acute respiratory distress syndrome (ARDS), multi-organ failure, and death [46].
SARS-CoV-2 is a large, spherical, enveloped, single stranded positive-sense ribonucleic acid (RNA) virus with genome size approximately 30 kilobase (kb) in length. There are four major structural proteins that form the backbone of the virus: The spike (S) protein, membrane (M) protein, envelope (E) protein, and nucleocapsid (N) protein. The unique structural protein, the spike (S) protein, which is present in abundance on the viral cell surface, plays a key role in its pathogenesis [47].
Pregnancy has always been associated with an increased risk of acquiring respiratory infection with higher morbidity and mortality than the nonpregnant subjects [48]. In a systematic review examining 2567 COVID-19 confirmed pregnancies with 746 deliveries, there were 3.4% women with maternal critical disease requiring mechanical ventilation support, 0.9% maternal death, and 21.8% preterm birth, primarily iatrogenic rather than spontaneous, and less than 1% perinatal death [49]. In another systematic review on 324 pregnancies with COVID-19, it was reported that up to 14% mothers with severe pneumonia required critical care, with a total of 9 cases of maternal deaths, 4 cases of spontaneous abortion, 4 cases of intrauterine fetal deaths, and 3 cases of neonatal death [50]. Brandt et al. (2020) conducted a matched case-control study involving 61 COVID-19 pregnancies matched to 2 controls by delivery date, and reported that the odds of adverse composite outcomes for mother and fetus were 3.4 times and 1.7 times higher among severe/critical COVID-19 cases than controls, respectively, with maternal advance age, obesity, Hispanic or Latino origin, and other medical comorbidities being some of the important factors driving a more severe clinical course. Reassuringly, pregnant women who were asymptomatic or had mild COVID-19 disease were observed to have benign outcomes [51].
The anatomical and physiological changes of the respiratory system as well as immunological and hormonal adaptation during pregnancy collectively make them more vulnerable to certain infections, including SARS-CoV-2 [52,53]. Anatomical and physiological changes in the maternal respiratory system include relaxation of rib ligaments, diaphragmatic elevation, and reduction in the functional residual capacity (FRC) of the lung initiated by the effects of progesterone, and hence ineffective airway clearance [53]. Functional ventilation and perfusion mismatch as a sequela of reduced FRC also increases the severity of respiratory infection. Besides, immunological modulation by a physiological shift to Th2 dominant environment and attenuation of Th1 cell-mediated immunity during pregnancy has increased viral infection risks. It does not only affect the viral clearance rate, but hastens the disease deterioration [54].
Notably, SARS-CoV-2 infects target host cells by binding to the cell membrane angiotensin-converting enzyme II (ACE2), facilitated by S protein priming proteases Type II transmembrane serine protease (TMPRSS2). ACE2 is a membrane-bound aminopeptidase enzyme that has a physiological role in degrading substances including angiotensins I and II, a key protective mechanism in regulating vascular and heart functions. It is found in most organs such as heart, lung, kidney, vessels, brain, and others, including the placenta [55]. The types of cell in placenta that express ACE2 are the syncytiotrophoblasts and cytotrophoblasts in villi, decidual stromal cells, decidual perivascular cells, and endothelial and vascular smooth muscle cells. The co-expression of the viral receptor ACE2 and TMPRSS2 in abundance in the human placenta theoretically may increase vulnerability of placenta and possibly fetus to SARS-CoV-2 infection [56,57].
Interestingly, subsequent studies pursued by Bloise et al. (2020) revealed that ACE2 and TMPRSS2 were differentially expressed at different stages of pregnancy. They observed that ACE2 and TMPRSS2 expressions in placenta were negatively correlated with gestational age, in which their expression levels in reducing trend from first trimester to second trimester placenta, and very low to almost undetectable in third trimester preterm and term placenta [57]. The authors concluded that the first trimester of pregnancy was possibly more vulnerable to SARS-CoV-2 transplacental transmission than in later stages of pregnancy [57]. Surprisingly, SARS-CoV-2 was not detected in the abortus/placenta in the few reported cases of first and second trimester miscarriages despite the mothers being tested positive for COVID-19 [19,58], but was found to be positive in amniotic fluid and infant born pre-term to a COVID-19-positive mother in the third trimester [59], even though, theoretically, third trimester infants should be protected from acquiring COVID-19 infection since there is a paucity of the required receptors present in the placenta.
In addition, Kotlyar et al. (2019), in their systematic review revealed that SARS-CoV-2 positivity detection rate from neonatal nasopharyngeal swab, cord blood, placenta samples, amniotic fluid, and serology was extant although low (ranges from 0–7.7%) [60]. It is possible that there is another alternate entry of SARS-CoV-2 into placenta cells beyond ACE2. Alternatively, it is possible that the presence of underdiagnosed/asymptomatic concurrent genital tract infection breaches the placental barrier and allows entry of the virus into amniotic cavity.
Viraemia is a prerequisite for transplacental transmission to occur. Emerging evidence showed that plasma viral load in COVID-19 cases was positively correlated with the disease severity [61]. Infants born to mothers with severe to critical COVID-19 diseases showed higher rates of SARS-CoV-2 positivity detected in the placenta and nasopharyngeal swab immediately after birth [26,62], supporting the viraemia hypothesis. Overall prevalence of viraemia in COVID-19 infected individuals, however, is low and transient [63], which makes placental seeding rather impossible and hence, the low rate of transplacental transmission. Arguably, the mere detection of viral RNA in the blood/serum does not reflect infectivity of a virus. Andersson et al. (2020) found that all their reverse transcription-polymerase chain reaction (RT-PCR)-positive clinical samples show neither viral replication nor display any cytopathic effect after inoculation in cell culture [64]. More studies are warranted to resolve these uncertainties.


This too:
https://dadamo.com/dangerous/2020/04/04/covid-19-ace2/ (how the body creates energy for growth is via ACE2 receptors which covid and covid vaxxes short-circuits.)
a whole debunking industry has been built on the ashes of the "legacy media" OH SHIT THE GOYIMZ FOUND US OUT QUICK FIND AND EXPLAINER!
 
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