MRNA contagious to the unvaccinated?

Lollipop2

Member
Joined
Nov 18, 2019
Messages
5,267
The fact that it's been going on for so long does make me think something went wrong for the dark controllers, who I think have been amassing power for a while. I do suspect some sort of power struggle near the top, be that White Hats vs. Black Hats, or fighting between Gray Hats, or what have you. It just feels like a desperation move to me.
+1 good news.
 

Vileplume

Member
Joined
Jun 10, 2020
Messages
1,697
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California
I emailed Ray about it. Here's his response:

Ray:
Our own DNA and RNA, proteins, exosomes, etc., are constantly being shed into our environment, so it seems extremely likely that any foreign DNA, RNA, and protein that’s in our blood will appear in our breath, sweat, urine, etc. Pfizer understood that, as indicated in this document. When people started worrying about it, a Pfizer representative said that the document doesn’t mean what it says.
Most people aren’t harmed by the corona virus, so the similar material coming from vaccinated people is likely to be equally harmless. The long range effects that might result from our incorporation of the gene that produces the spike protein would be likely to include inflammation, that would only become a serious problem when our resistance was lowered, by sickness or aging. Prolonged inflammation is carcinogenic, and our ACE2 enzyme (which is inactivated by the spike protein), is one of our protective anti-cancer factors (articles below).
Ideally, vaccinated people would be quarantined until they could show that they weren’t shedding the harmful material, but the govenments aren’t behaving rationally.


https://media.tghn.org/medialibrary/2020/11/C4591001_Clinical_Protocol_Nov2020_Pfizer_BioNTech.pdf
PF-07302048 (BNT162 RNA-Based COVID-19 Vaccines) Protocol C4591001
A PHASE 1/2/3, PLACEBO-CONTROLLED, RANDOMIZED, OBSERVER-BLIND, DOSE-FINDING STUDY TO EVALUATE THE SAFETY, TOLERABILITY, IMMUNOGENICITY, AND EFFICACY OF SARS-COV-2 RNA VACCINE CANDIDATES AGAINST COVID-19 IN HEALTHY INDIVIDUALS
Study Sponsor:
Study Conducted By:
Study Intervention Number:
Study Intervention Name:
US IND Number:
EudraCT Number:
Protocol Number:
BioNTech
Pfizer
PF-07302048
RNA-Based COVID-19 Vaccines 19736
2020-002641-42 C4591001
1/2/3
Phase:
Short Title: A Phase 1/2/3 Study to Evaluate the Safety, Tolerability, Immunogenicity, and
Efficacy of RNA Vaccine Candidates Against COVID-19 in Healthy Individuals


=============

(page 67, …)

8.3.5. Exposure During Pregnancy or Breastfeeding, and Occupational Exposure
Exposure to the study intervention under study during pregnancy or breastfeeding and occupational exposure are reportable to Pfizer Safety within 24 hours of investigator awareness.
8.3.5.1. Exposure During Pregnancy
An EDP occurs if:
  • A female participant is found to be pregnant while receiving or after discontinuing study intervention.
  • A male participant who is receiving or has discontinued study intervention exposes a female partner prior to or around the time of conception.
  • A female is found to be pregnant while being exposed or having been exposed to study intervention due to environmental exposure. Below are examples of environmental exposure during pregnancy:
• A female family member or healthcare provider reports that she is pregnant after having been exposed to the study intervention by inhalation or skin contact.
Page 67
PF-07302048 (BNT162 RNA-Based COVID-19 Vaccines) Protocol C4591001
• A male family member or healthcare provider who has been exposed to the study intervention by inhalation or skin contact then exposes his female partner prior to or around the time of conception.
The investigator must report EDP to Pfizer Safety within 24 hours of the investigator’s awareness, irrespective of whether an SAE has occurred. The initial information submitted should include the anticipated date of delivery (see below for information related to termination of pregnancy).
  • If EDP occurs in a participant or a participant’s partner, the investigator must report this information to Pfizer Safety on the Vaccine SAE Report Form and an EDP Supplemental Form, regardless of whether an SAE has occurred. Details of the pregnancy will be collected after the start of study intervention and until 6 months after the last dose of study intervention.
  • If EDP occurs in the setting of environmental exposure, the investigator must report information to Pfizer Safety using the Vaccine SAE Report Form and EDP Supplemental Form. Since the exposure information does not pertain to the participant enrolled in the study, the information is not recorded on a CRF; however, a copy of the completed Vaccine SAE Report Form is maintained in the investigator site file.
    Follow-up is conducted to obtain general information on the pregnancy and its outcome for all EDP reports with an unknown outcome. The investigator will follow the pregnancy until completion (or until pregnancy termination) and notify Pfizer Safety of the outcome as a follow-up to the initial EDP Supplemental Form. In the case of a live birth, the structural integrity of the neonate can be assessed at the time of birth. In the event of a termination, the reason(s) for termination should be specified and, if clinically possible, the structural integrity of the terminated fetus should be assessed by gross visual inspection (unless preprocedure test findings are conclusive for a congenital anomaly and the findings are reported).
    Abnormal pregnancy outcomes are considered SAEs. If the outcome of the pregnancy meets the criteria for an SAE (ie, ectopic pregnancy, spontaneous abortion, intrauterine fetal demise, neonatal death, or congenital anomaly), the investigator should follow the procedures for reporting SAEs. Additional information about pregnancy outcomes that are reported to Pfizer Safety as SAEs follows:
  • Spontaneous abortion including miscarriage and missed abortion;
  • Neonatal deaths that occur within 1 month of birth should be reported, without regard to causality, as SAEs. In addition, infant deaths after 1 month should be reported as SAEs when the investigator assesses the infant death as related or possibly related to exposure to the study intervention.
Page 68
PF-07302048 (BNT162 RNA-Based COVID-19 Vaccines) Protocol C4591001
Additional information regarding the EDP may be requested by the sponsor. Further follow-up of birth outcomes will be handled on a case-by-case basis (eg, follow-up on preterm infants to identify developmental delays). In the case of paternal exposure, the investigator will provide the participant with the Pregnant Partner Release of Information Form to deliver to his partner. The investigator must document in the source documents that the participant was given the Pregnant Partner Release of Information Form to provide to his partner.
8.3.5.2. Exposure During Breastfeeding
An exposure during breastfeeding occurs if:
  • A female participant is found to be breastfeeding while receiving or after discontinuing study intervention.
  • A female is found to be breastfeeding while being exposed or having been exposed to study intervention (ie, environmental exposure). An example of environmental exposure during breastfeeding is a female family member or healthcare provider who reports that she is breastfeeding after having been exposed to the study intervention by inhalation or skin contact.
    The investigator must report exposure during breastfeeding to Pfizer Safety within 24 hours of the investigator’s awareness, irrespective of whether an SAE has occurred. The information must be reported using the Vaccine SAE Report Form. When exposure during breastfeeding occurs in the setting of environmental exposure, the exposure information does not pertain to the participant enrolled in the study, so the information is not recorded on a CRF. However, a copy of the completed Vaccine SAE Report Form is maintained in the investigator site file.
    An exposure during breastfeeding report is not created when a Pfizer drug specifically approved for use in breastfeeding women (eg, vitamins) is administered in accord with authorized use. However, if the infant experiences an SAE associated with such a drug, the SAE is reported together with the exposure during breastfeeding.
    8.3.5.3. Occupational Exposure
    An occupational exposure occurs when a person receives unplanned direct contact with the study intervention, which may or may not lead to the occurrence of an AE. Such persons may include healthcare providers, family members, and other roles that are involved in the trial participant’s care.
    The investigator must report occupational exposure to Pfizer Safety within 24 hours of the investigator’s awareness, regardless of whether there is an associated SAE. The information must be reported using the Vaccine SAE Report Form. Since the information does not pertain to a participant enrolled in the study, the information is not recorded on a CRF; however, a copy of the completed Vaccine SAE Report Form is maintained in the investigator site file.
Page 69

==============================

SARS-CoV-2 RNA reverse-transcribed and integrated into the human genome
Liguo Zhang, Alexsia Richards, Andrew Khalil, Emile Wogram, Haiting Ma, Richard A Young, Rudolf Jaenisch
Abstract
Prolonged SARS-CoV-2 RNA shedding and recurrence of PCR-positive tests have been widely reported in patients after recovery, yet these patients most commonly are non-infectious. Here we investigated the possibility that SARS-CoV-2 RNAs can be reverse-transcribed and integrated into the human genome and that transcription of the integrated sequences might account for PCR-positive tests. In support of this hypothesis, we found chimeric transcripts consisting of viral fused to cellular sequences in published data sets of SARS-CoV-2 infected cultured cells and primary cells of patients, consistent with the transcription of viral sequences integrated into the genome. To experimentally corroborate the possibility of viral retro-integration, we describe evidence that SARS-CoV-2 RNAs can be reverse transcribed in human cells by reverse transcriptase (RT) from LINE-1 elements or by HIV-1 RT, and that these DNA sequences can be integrated into the cell genome and subsequently be transcribed. Human endogenous LINE-1 expression was induced upon SARS-CoV-2 infection or by cytokine exposure in cultured cells, suggesting a molecular mechanism for SARS-CoV-2 retro-integration in patients. This novel feature of SARS-CoV-2 infection may explain why patients can continue to produce viral RNA after recovery and suggests a new aspect of RNA virus replication.

from Wikipedia:
In cellular life
Self-replicating stretches of eukaryotic genomes known as retrotransposons utilize reverse transcriptase to move from one position in the genome to another via an RNA intermediate. They are found abundantly in the genomes of plants and animals. Telomerase is another reverse transcriptase found in many eukaryotes, including humans, which carries its own RNA template; this RNA is used as a template for DNA replication.[15]
Initial reports of reverse transcriptase in prokaryotes came as far back as 1971 in France (Beljanski et al., 1971a, 1972) and a few years later in the USSR (Romashchenko 1977[16]). These have since been broadly described as part of bacterial Retrons, distinct sequences that code for reverse transcriptase, and are used in the synthesis of msDNA. In order to initiate synthesis of DNA, a primer is needed. In bacteria, the primer is synthesized during replication.[17]
Valerian Dolja of Oregon State argues that viruses, due to their diversity, have played an evolutionary role in the development of cellular life, with reverse transcriptase playing a central role.[18]


1
Oncol Rep. 2011 Nov;26(5):1157-64.
Overexpression of ACE2 produces antitumor effects via inhibition of angiogenesis and tumor cell invasion in vivo and in vitro
Yun Feng 1 , Lei Ni, Huanying Wan, Liang Fan, Xiaochun Fei, Qinyun Ma, Beili Gao, Yi Xiang, Jiaming Che, Qingyun Li
Angiotensin II (AngII) is a multifunctional bioactive peptide in the renin-angiotensin system (RAS). Angiotensin-converting enzyme 2 (ACE2) is a newly identified component of RAS. The role of AngII and ACE2 in the metastasis of non-small cell lung cancer (NSCLC) and the effects on matrix metalloproteinases (MMPs) are still unknown. In the present study, the anti-invasive effect and mechanism of ACE2 were investigated in vitro and in vivo. Results of a transwell assay showed that the overexpression of ACE2 reduces the invasive ability of A549 cells in vitro. According to the results of qRT-PCR and western blot analysis, the inhibitory role of ACE2 was mediated through the down-regulation of MMP-2 and MMP-9. Additionally, we confirmed that the overexpression of ACE2 inhibited cell growth and VEGFa production while simultaneously suppressing ACE and angiotensin II type 1 receptor (AT1R) expression in human lung cancer xenografts. These results suggest that the overexpression of ACE2 may potentially suppress the invasion and angiogenesis of NSCLC.

2
J Exp Clin Cancer Res. 2019 Apr 25;38(1):173.
ACE2 inhibits breast cancer angiogenesis via suppressing the VEGFa/VEGFR2/ERK pathway
Qi Zhang 1 2 , Sihong Lu 1 3 , Tianfu Li 1 , Liang Yu 1 , Yunjian Zhang 1 , Huijuan Zeng 1 , Xueke Qian 4 , Jiong Bi 5 , Ying Lin 6
Free PMC article
Abstract
Background: Breast cancer angiogenesis is key for metastasis and predicts a poor prognosis. Angiotensin-converting enzyme 2 (ACE2), as a member of the renin-angiotensin system (RAS), was reported to restrain the progression of hepatocellular carcinoma (HCC) and non-small cell lung cancer (NSCLC) through inhibiting angiogenesis. However, the relationship between ACE2 and breast cancer angiogenesis remains unclear.
Methods: The prognosis and relative gene selection were analysed using the GEPIA, GEO, TCGA and STRING databases. ACE2 expression in breast cancer tissue was estimated by reverse transcription-quantitative polymerase chain reaction (qPCR). Breast cancer cell migration, proliferation and angiogenesis were assessed by Transwell migration, proliferation, tube formation, and wound healing assays. The expression of vascular endothelial growth factor A (VEGFa) was detected by qPCR and Western blotting. The phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2), mitogen-activated protein kinase 1/2 (MEK1/2), and extracellular signal-regulated protein kinase 1/2 (ERK1/2) was examined by Western blotting. Breast cancer metastasis and angiogenesis in vivo were measured using a zebrafish model.
Results: ACE2 was downregulated in breast cancer patients. Patients with higher ACE2 expression had longer relapse-free survival (RFS). In vitro, ACE2 inhibited breast cancer migration. Meanwhile, ACE2 in breast cancer cells inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, tube formation and migration. In the zebrafish model, ACE2 inhibited breast cancer cell metastasis, as demonstrated by analyses of the number of disseminated foci and the metastatic distance. Neo-angiogenesis was also decreased by ACE2. ACE2 downregulated the expression of VEGFa in breast cancer cells. Furthermore, ACE2 in breast cancer cells inactivated the phosphorylation of VEGFR2, MEK1/2, and ERK1/2 in HUVECs.
Conclusions: Our findings suggest that ACE2, as a potential resister to breast cancer, might inhibit breast cancer angiogenesis through the VEGFa/VEGFR2/ERK pathway.
Trial registration: Retrospectively registered.
Keywords: ACE2; Angiogenesis; Breast cancer; ERK; VEGFR2; VEGFa.
Conflict of interest statement
Ethics approval and consent to participate
Approval and consent obtained for the use of human tissue were obtained from the Institutional Research Ethics Committee of the First Affiliated Hospital of Sun Yat-sen University.
Approval for all the zebrafish experiments was obtained from Sun Yat-sen University Animal Care and Use Committee of the Zebrafish Model Animal Facility, Institute of Clinical and Translational Research, Sun Yat-sen University.

3
Tohoku J Exp Med. 2009 Feb;217(2):123-31.
Decreased expression of angiotensin-converting enzyme 2 in pancreatic ductal adenocarcinoma is associated with tumor progression
Lin Zhou 1 , Ruifeng Zhang, Weiyan Yao, Jiancheng Wang, Aihua Qian, Minmin Qiao, Yongping Zhang, Yaozong Yuan
Free article
Angiotensin II (ANG II), the biologically active peptide of the renin-angiotensin system (RAS), is generated by angiotensin-converting enzyme (ACE) and is a regulator of cardiovascular homeostasis. Recently, there has been increasing evidence that ANG II is involved in the regulation of cell proliferation and migration, as well as angiogenesis via the ANG II-type 1 receptor (AT1R). These findings suggest that the ACE-ANG II-AT1R pathway is related to cancer biology. Previous reports have shown that ACE is preferentially expressed in pancreatic ductal adenocarcinoma (PDAC) tissues. Recently a homologue of ACE, angiotensin-converting enzyme 2 (ACE2), was reported to counterbalance the function of ACE, but the expression and role of ACE2 in PDAC are still unclear. In the present study, we analyzed the expression of ACE2 in invasive human PDAC and surrounding non-malignant tissues by Western blot analysis and immunohistochemistry. The ANG II concentration in homogenates of pancreatic tissues was measured with ELISA, and ACE2 protein was detected by Western blot analysis in BxPC3 and SW1990 human pancreatic ductal cancer cells. We have shown for the first time that the expression of ACE2 is decreased in PDAC tissues, in which ANG II was accumulated. Treatment of BxPC3 and SW1990 cells with ANG II decreased the expression of ACE2. Therefore, ANG II may contribute to the down-regulation of ACE2. Moreover, reduction of ACE2 expression by RNA interference promoted the proliferation of cultured pancreatic cancer cells. These findings suggest that ACE2 may have clinical potential as a novel molecular target for the treatment of PDAC.

4
Oncol Rep. 2010 Apr;23(4):941-8.
The angiotensin-converting enzyme 2 in tumor growth and tumor-associated angiogenesis in non-small cell lung cancer
Yun Feng 1 , Huanying Wan, Jialin Liu, Ruifeng Zhang, Qinyun Ma, Bing Han, Yi Xiang, Jiaming Che, Huangming Cao, Xiaochun Fei, Weicheng Qiu
Angiotensin II (AngII) is a multifunctional bioactive peptide and previous studies have shown that the renin-angiotensin system (RAS) of both host and tumor are important in tumor growth and angiogenesis in lung cancer. Angiotensin-converting enzyme 2 (ACE2) is a newly identified component of RAS, with 42% amino acid homology to ACE. However, the expression and function of ACE2 in non-small cell lung cancer (NSCLC) are still unclear. In the present study, we analyzed ACE2 expression in NSCLC tissue by Western blot analysis and immunohistochemistry. AngII concentrations in the tissue homogenate were also detected using radio-immunoassay. We also examined the function of ACE2 by transducing A549 cells with MSCV-ACE2. We have shown for the first time that ACE2 expression decreased in NSCLC tissue in which AngII was higher than the matching non-malignant tissues. A concentration of 10(-6) mol/l of AngII significantly increased expression of vascular endothelial growth factor a (VEGFa) and AT1-R and decreased ACE2 expression. We also found that overexpression of ACE2 may have a protective effect by inhibiting cell growth and VEGFa production in vitro. ACE2 may become a target of novel strategies to treat NSCLC.
Cited by 33 articles

5
Oncol Rep. 2016 Sep;36(3):1403-10.
ACE2 overexpression inhibits acquired platinum resistance-induced tumor angiogenesis in NSCLC
Qijian Cheng 1 , Ling Zhou 1 , Jianping Zhou 1 , Huanying Wan 1 , Qingyun Li 1 , Yun Feng 1
Angiotensin II (AngII) is a multifunctional bioactive peptide in the renin-angiotensin system (RAS). Angiotensin-converting enzyme 2 (ACE2) is a newly identified component of RAS. We previously reported that ACE2 overexpression may inhibit cell growth and vascular endothelial growth factor (VEGF) production in vitro and in vivo. In the present study, we investigated the effect of ACE2 on tumor-associated angiogen-esis after the development of acquired platinum resistance in non-small cell lung cancer (NSCLC). Four NSCLC cell lines, A549, LLC, A549-DDP and LLC-DDP, were used in vitro, while A549 and A549-DDP cells were used in vivo. A549-DDP and LLC-DDP cells were newly established at our institution as acquired platinum-resistant sublines by culturing the former parent cells in cisplatin (CDDP)-containing conditioned medium for 6 months. These platinum-resistant cells showed significantly higher angiotensin II type 1 receptor (AT1R), ACE and VEGF production and lower ACE2 expression than their corresponding parent cells. We showed that ACE2 overexpression inhibited the production of VEGF in vitro and in vivo compared to their corresponding parent cells. We also found that ACE2 overexpression reduced the expression of AT1R and ACE. Additionally, we confirmed that ACE2 overexpres-sion inhibited cell growth and VEGF production while simultaneously suppressing ACE and AT1R expression in human lung cancer xenografts. Our findings indicate that ACE2 overexpression may potentially suppress angiogenesis in NSCLC after the development of acquired platinum resistance.

6
Oncol Rep. 2013 Jun;29(6):2408-14.
doi: 10.3892/or.2013.2370. Epub 2013 Mar 29.
Angiotensin-converting enzyme 2 attenuates the metastasis of non-small cell lung cancer through inhibition of epithelial-mesenchymal transition
Yan-Rong Qian 1 , Yi Guo, Huan-Ying Wan, Liang Fan, Yun Feng, Lei Ni, Yi Xiang, Qing-Yun Li
Angiotensin-converting enzyme 2 (ACE2) is a key enzyme of the renin-angiotensin system (RAS). ACE2 plays a critical counterbalancing role by degrading angiotensin II (Ang II) to Ang 1-7. Recent studies suggest that RAS influences tumor growth and development by its paracrine effects on the tumor microenvironment. Epithelial‑mesenchymal transition (EMT) is now thought to be a process that plays a fundamental role in tumor progression and metastasis. In the present study, we investigated the role of ACE2 in lung cancer metastasis and the mechanism of EMT. This is the first study to elucidate the mechanism through which the overexpression of ACE2 in the A549 lung cancer cell line decreases metastasis formation in vivo and upregulates the expression of E-cadherin both in vitro and in vivo. We also observed the downregulation of vimentin, which supports a role of ACE2 in influencing EMT in lung cancer. Further analysis indicated that ACE2 abrogated the upregulation of TGF-β1-induced EMT markers, such as vimentin and α-smooth muscle actin (αSMA) in vitro in A549 cells. Finally, exposing A549 cells stably expressing ACE2 to DX600, an inhibitor of ACE2, recovered the sensitivity of lung cancer cells to TGF-β1-mediated induction of EMT. Our study demonstrated that ACE2 attenuated the metastasis of lung cancer and may serve as a target for new strategies to inhibit EMT in cancer cells.

7
Comparative Study
Lab Invest. 2007 Feb;87(2):189-98.
Roles for host and tumor angiotensin II type 1 receptor in tumor growth and tumor-associated angiogenesis
Nozomi Imai 1 , Tatsuo Hashimoto, Minoru Kihara, Shin-ichiro Yoshida, Ichiro Kawana, Takuya Yazawa, Hitoshi Kitamura, Satoshi Umemura
Angiotensin II (AII) is a multifunctional bioactive peptide, and host renin-angiotensin system (RAS) is closely associated with tumor growth. Recent reports have described that AII is a proangiogenic growth factor, and that Angiotensin II type 1 (AT1) receptor antagonists reduce tumor growth and tumor-associated angiogenesis. In this paper, we investigated the participation of AT1 receptor-signaling in cancer progression using murine Lewis lung carcinoma (LLC) cells, which express AT1 receptor, and AT1a receptor gene-deficient (AT1a-/-) mice. When LLC cells were implanted subcutaneously into wild-type (WT) mice, developed tumors showed intensive angiogenesis with an induction of vascular endothelial growth factor (VEGF) a. Compared with WT mice, tumor growth and tumor-associated angiogenesis was reduced in AT1a-/- mice with reduced expression of VEGFa. In AT1a-/- mice, administration of the AT1 receptor antagonist, TCV-116, showed further reductions of tumor growth, tumor-associated angiogenesis, and VEGFa expression. In vitro study, the expression of VEGFa mRNA and the production of VEGFa protein in LLC cells were significantly increased by AII, which were cancelled by AT1 receptor antagonist, CV-11974. Although the expression of other angiogenic factors, such as angiopoietin-1, angiopoietin-2, epidermal growth factor, and VEGF receptor 2 mRNA, was also investigated in tumor tissues, the expression of VEGFa was most correlated with tumor size among those other angiogenic factors. VEGFa induction by AT1 receptor-signaling in both host and tumor tissues is one of key regulators of tumor growth and tumor-associated angiogenesis. In conclusion, tumor tissue RAS as well as host tissue RAS were found to have an important role in tumor growth. AT1 receptor-signaling blockade may be a novel and effective target in the treatment of cancer.

SARS-CoV-2 RNA can be reverse-transcribed to be part of chimeric viral-human genome

================================================

CDC: 4,178 Americans DEAD Following Experimental COVID Injections – Deaths from COVID Shots now Equal 20 Years of Recorded Deaths Following Vaccines Since 2001


View: https://rumble.com/vgerov-dr.-sucharit-bhakdi-warns-covid-shots-to-decimate-world-population.html


New Report sheds light on Vaccine Doomsday Cult


View: https://www.bitchute.com/video/cdKu2RXGAWyu/



View: https://www.bitchute.com/video/ecOpzGNqNbgZ/
 

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Lollipop2

Member
Joined
Nov 18, 2019
Messages
5,267
I emailed Ray about it. Here's his response:

Ray:
Our own DNA and RNA, proteins, exosomes, etc., are constantly being shed into our environment, so it seems extremely likely that any foreign DNA, RNA, and protein that’s in our blood will appear in our breath, sweat, urine, etc. Pfizer understood that, as indicated in this document. When people started worrying about it, a Pfizer representative said that the document doesn’t mean what it says.
Most people aren’t harmed by the corona virus, so the similar material coming from vaccinated people is likely to be equally harmless. The long range effects that might result from our incorporation of the gene that produces the spike protein would be likely to include inflammation, that would only become a serious problem when our resistance was lowered, by sickness or aging. Prolonged inflammation is carcinogenic, and our ACE2 enzyme (which is inactivated by the spike protein), is one of our protective anti-cancer factors (articles below).
Ideally, vaccinated people would be quarantined until they could show that they weren’t shedding the harmful material, but the govenments aren’t behaving rationally.


https://media.tghn.org/medialibrary/2020/11/C4591001_Clinical_Protocol_Nov2020_Pfizer_BioNTech.pdf
PF-07302048 (BNT162 RNA-Based COVID-19 Vaccines) Protocol C4591001
A PHASE 1/2/3, PLACEBO-CONTROLLED, RANDOMIZED, OBSERVER-BLIND, DOSE-FINDING STUDY TO EVALUATE THE SAFETY, TOLERABILITY, IMMUNOGENICITY, AND EFFICACY OF SARS-COV-2 RNA VACCINE CANDIDATES AGAINST COVID-19 IN HEALTHY INDIVIDUALS
Study Sponsor:
Study Conducted By:
Study Intervention Number:
Study Intervention Name:
US IND Number:
EudraCT Number:
Protocol Number:
BioNTech
Pfizer
PF-07302048
RNA-Based COVID-19 Vaccines 19736
2020-002641-42 C4591001
1/2/3
Phase:
Short Title: A Phase 1/2/3 Study to Evaluate the Safety, Tolerability, Immunogenicity, and
Efficacy of RNA Vaccine Candidates Against COVID-19 in Healthy Individuals


=============

(page 67, …)

8.3.5. Exposure During Pregnancy or Breastfeeding, and Occupational Exposure
Exposure to the study intervention under study during pregnancy or breastfeeding and occupational exposure are reportable to Pfizer Safety within 24 hours of investigator awareness.
8.3.5.1. Exposure During Pregnancy
An EDP occurs if:
  • A female participant is found to be pregnant while receiving or after discontinuing study intervention.
  • A male participant who is receiving or has discontinued study intervention exposes a female partner prior to or around the time of conception.
  • A female is found to be pregnant while being exposed or having been exposed to study intervention due to environmental exposure. Below are examples of environmental exposure during pregnancy:
• A female family member or healthcare provider reports that she is pregnant after having been exposed to the study intervention by inhalation or skin contact.
Page 67
PF-07302048 (BNT162 RNA-Based COVID-19 Vaccines) Protocol C4591001
• A male family member or healthcare provider who has been exposed to the study intervention by inhalation or skin contact then exposes his female partner prior to or around the time of conception.
The investigator must report EDP to Pfizer Safety within 24 hours of the investigator’s awareness, irrespective of whether an SAE has occurred. The initial information submitted should include the anticipated date of delivery (see below for information related to termination of pregnancy).
  • If EDP occurs in a participant or a participant’s partner, the investigator must report this information to Pfizer Safety on the Vaccine SAE Report Form and an EDP Supplemental Form, regardless of whether an SAE has occurred. Details of the pregnancy will be collected after the start of study intervention and until 6 months after the last dose of study intervention.
  • If EDP occurs in the setting of environmental exposure, the investigator must report information to Pfizer Safety using the Vaccine SAE Report Form and EDP Supplemental Form. Since the exposure information does not pertain to the participant enrolled in the study, the information is not recorded on a CRF; however, a copy of the completed Vaccine SAE Report Form is maintained in the investigator site file.
    Follow-up is conducted to obtain general information on the pregnancy and its outcome for all EDP reports with an unknown outcome. The investigator will follow the pregnancy until completion (or until pregnancy termination) and notify Pfizer Safety of the outcome as a follow-up to the initial EDP Supplemental Form. In the case of a live birth, the structural integrity of the neonate can be assessed at the time of birth. In the event of a termination, the reason(s) for termination should be specified and, if clinically possible, the structural integrity of the terminated fetus should be assessed by gross visual inspection (unless preprocedure test findings are conclusive for a congenital anomaly and the findings are reported).
    Abnormal pregnancy outcomes are considered SAEs. If the outcome of the pregnancy meets the criteria for an SAE (ie, ectopic pregnancy, spontaneous abortion, intrauterine fetal demise, neonatal death, or congenital anomaly), the investigator should follow the procedures for reporting SAEs. Additional information about pregnancy outcomes that are reported to Pfizer Safety as SAEs follows:
  • Spontaneous abortion including miscarriage and missed abortion;
  • Neonatal deaths that occur within 1 month of birth should be reported, without regard to causality, as SAEs. In addition, infant deaths after 1 month should be reported as SAEs when the investigator assesses the infant death as related or possibly related to exposure to the study intervention.
Page 68
PF-07302048 (BNT162 RNA-Based COVID-19 Vaccines) Protocol C4591001
Additional information regarding the EDP may be requested by the sponsor. Further follow-up of birth outcomes will be handled on a case-by-case basis (eg, follow-up on preterm infants to identify developmental delays). In the case of paternal exposure, the investigator will provide the participant with the Pregnant Partner Release of Information Form to deliver to his partner. The investigator must document in the source documents that the participant was given the Pregnant Partner Release of Information Form to provide to his partner.
8.3.5.2. Exposure During Breastfeeding
An exposure during breastfeeding occurs if:
  • A female participant is found to be breastfeeding while receiving or after discontinuing study intervention.
  • A female is found to be breastfeeding while being exposed or having been exposed to study intervention (ie, environmental exposure). An example of environmental exposure during breastfeeding is a female family member or healthcare provider who reports that she is breastfeeding after having been exposed to the study intervention by inhalation or skin contact.
    The investigator must report exposure during breastfeeding to Pfizer Safety within 24 hours of the investigator’s awareness, irrespective of whether an SAE has occurred. The information must be reported using the Vaccine SAE Report Form. When exposure during breastfeeding occurs in the setting of environmental exposure, the exposure information does not pertain to the participant enrolled in the study, so the information is not recorded on a CRF. However, a copy of the completed Vaccine SAE Report Form is maintained in the investigator site file.
    An exposure during breastfeeding report is not created when a Pfizer drug specifically approved for use in breastfeeding women (eg, vitamins) is administered in accord with authorized use. However, if the infant experiences an SAE associated with such a drug, the SAE is reported together with the exposure during breastfeeding.
    8.3.5.3. Occupational Exposure
    An occupational exposure occurs when a person receives unplanned direct contact with the study intervention, which may or may not lead to the occurrence of an AE. Such persons may include healthcare providers, family members, and other roles that are involved in the trial participant’s care.
    The investigator must report occupational exposure to Pfizer Safety within 24 hours of the investigator’s awareness, regardless of whether there is an associated SAE. The information must be reported using the Vaccine SAE Report Form. Since the information does not pertain to a participant enrolled in the study, the information is not recorded on a CRF; however, a copy of the completed Vaccine SAE Report Form is maintained in the investigator site file.
Page 69

==============================

SARS-CoV-2 RNA reverse-transcribed and integrated into the human genome
Liguo Zhang, Alexsia Richards, Andrew Khalil, Emile Wogram, Haiting Ma, Richard A Young, Rudolf Jaenisch
Abstract
Prolonged SARS-CoV-2 RNA shedding and recurrence of PCR-positive tests have been widely reported in patients after recovery, yet these patients most commonly are non-infectious. Here we investigated the possibility that SARS-CoV-2 RNAs can be reverse-transcribed and integrated into the human genome and that transcription of the integrated sequences might account for PCR-positive tests. In support of this hypothesis, we found chimeric transcripts consisting of viral fused to cellular sequences in published data sets of SARS-CoV-2 infected cultured cells and primary cells of patients, consistent with the transcription of viral sequences integrated into the genome. To experimentally corroborate the possibility of viral retro-integration, we describe evidence that SARS-CoV-2 RNAs can be reverse transcribed in human cells by reverse transcriptase (RT) from LINE-1 elements or by HIV-1 RT, and that these DNA sequences can be integrated into the cell genome and subsequently be transcribed. Human endogenous LINE-1 expression was induced upon SARS-CoV-2 infection or by cytokine exposure in cultured cells, suggesting a molecular mechanism for SARS-CoV-2 retro-integration in patients. This novel feature of SARS-CoV-2 infection may explain why patients can continue to produce viral RNA after recovery and suggests a new aspect of RNA virus replication.

from Wikipedia:
In cellular life
Self-replicating stretches of eukaryotic genomes known as retrotransposons utilize reverse transcriptase to move from one position in the genome to another via an RNA intermediate. They are found abundantly in the genomes of plants and animals. Telomerase is another reverse transcriptase found in many eukaryotes, including humans, which carries its own RNA template; this RNA is used as a template for DNA replication.[15]
Initial reports of reverse transcriptase in prokaryotes came as far back as 1971 in France (Beljanski et al., 1971a, 1972) and a few years later in the USSR (Romashchenko 1977[16]). These have since been broadly described as part of bacterial Retrons, distinct sequences that code for reverse transcriptase, and are used in the synthesis of msDNA. In order to initiate synthesis of DNA, a primer is needed. In bacteria, the primer is synthesized during replication.[17]
Valerian Dolja of Oregon State argues that viruses, due to their diversity, have played an evolutionary role in the development of cellular life, with reverse transcriptase playing a central role.[18]


1
Oncol Rep. 2011 Nov;26(5):1157-64.
Overexpression of ACE2 produces antitumor effects via inhibition of angiogenesis and tumor cell invasion in vivo and in vitro
Yun Feng 1 , Lei Ni, Huanying Wan, Liang Fan, Xiaochun Fei, Qinyun Ma, Beili Gao, Yi Xiang, Jiaming Che, Qingyun Li
Angiotensin II (AngII) is a multifunctional bioactive peptide in the renin-angiotensin system (RAS). Angiotensin-converting enzyme 2 (ACE2) is a newly identified component of RAS. The role of AngII and ACE2 in the metastasis of non-small cell lung cancer (NSCLC) and the effects on matrix metalloproteinases (MMPs) are still unknown. In the present study, the anti-invasive effect and mechanism of ACE2 were investigated in vitro and in vivo. Results of a transwell assay showed that the overexpression of ACE2 reduces the invasive ability of A549 cells in vitro. According to the results of qRT-PCR and western blot analysis, the inhibitory role of ACE2 was mediated through the down-regulation of MMP-2 and MMP-9. Additionally, we confirmed that the overexpression of ACE2 inhibited cell growth and VEGFa production while simultaneously suppressing ACE and angiotensin II type 1 receptor (AT1R) expression in human lung cancer xenografts. These results suggest that the overexpression of ACE2 may potentially suppress the invasion and angiogenesis of NSCLC.

2
J Exp Clin Cancer Res. 2019 Apr 25;38(1):173.
ACE2 inhibits breast cancer angiogenesis via suppressing the VEGFa/VEGFR2/ERK pathway
Qi Zhang 1 2 , Sihong Lu 1 3 , Tianfu Li 1 , Liang Yu 1 , Yunjian Zhang 1 , Huijuan Zeng 1 , Xueke Qian 4 , Jiong Bi 5 , Ying Lin 6
Free PMC article
Abstract
Background: Breast cancer angiogenesis is key for metastasis and predicts a poor prognosis. Angiotensin-converting enzyme 2 (ACE2), as a member of the renin-angiotensin system (RAS), was reported to restrain the progression of hepatocellular carcinoma (HCC) and non-small cell lung cancer (NSCLC) through inhibiting angiogenesis. However, the relationship between ACE2 and breast cancer angiogenesis remains unclear.
Methods: The prognosis and relative gene selection were analysed using the GEPIA, GEO, TCGA and STRING databases. ACE2 expression in breast cancer tissue was estimated by reverse transcription-quantitative polymerase chain reaction (qPCR). Breast cancer cell migration, proliferation and angiogenesis were assessed by Transwell migration, proliferation, tube formation, and wound healing assays. The expression of vascular endothelial growth factor A (VEGFa) was detected by qPCR and Western blotting. The phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2), mitogen-activated protein kinase 1/2 (MEK1/2), and extracellular signal-regulated protein kinase 1/2 (ERK1/2) was examined by Western blotting. Breast cancer metastasis and angiogenesis in vivo were measured using a zebrafish model.
Results: ACE2 was downregulated in breast cancer patients. Patients with higher ACE2 expression had longer relapse-free survival (RFS). In vitro, ACE2 inhibited breast cancer migration. Meanwhile, ACE2 in breast cancer cells inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, tube formation and migration. In the zebrafish model, ACE2 inhibited breast cancer cell metastasis, as demonstrated by analyses of the number of disseminated foci and the metastatic distance. Neo-angiogenesis was also decreased by ACE2. ACE2 downregulated the expression of VEGFa in breast cancer cells. Furthermore, ACE2 in breast cancer cells inactivated the phosphorylation of VEGFR2, MEK1/2, and ERK1/2 in HUVECs.
Conclusions: Our findings suggest that ACE2, as a potential resister to breast cancer, might inhibit breast cancer angiogenesis through the VEGFa/VEGFR2/ERK pathway.
Trial registration: Retrospectively registered.
Keywords: ACE2; Angiogenesis; Breast cancer; ERK; VEGFR2; VEGFa.
Conflict of interest statement
Ethics approval and consent to participate
Approval and consent obtained for the use of human tissue were obtained from the Institutional Research Ethics Committee of the First Affiliated Hospital of Sun Yat-sen University.
Approval for all the zebrafish experiments was obtained from Sun Yat-sen University Animal Care and Use Committee of the Zebrafish Model Animal Facility, Institute of Clinical and Translational Research, Sun Yat-sen University.

3
Tohoku J Exp Med. 2009 Feb;217(2):123-31.
Decreased expression of angiotensin-converting enzyme 2 in pancreatic ductal adenocarcinoma is associated with tumor progression
Lin Zhou 1 , Ruifeng Zhang, Weiyan Yao, Jiancheng Wang, Aihua Qian, Minmin Qiao, Yongping Zhang, Yaozong Yuan
Free article
Angiotensin II (ANG II), the biologically active peptide of the renin-angiotensin system (RAS), is generated by angiotensin-converting enzyme (ACE) and is a regulator of cardiovascular homeostasis. Recently, there has been increasing evidence that ANG II is involved in the regulation of cell proliferation and migration, as well as angiogenesis via the ANG II-type 1 receptor (AT1R). These findings suggest that the ACE-ANG II-AT1R pathway is related to cancer biology. Previous reports have shown that ACE is preferentially expressed in pancreatic ductal adenocarcinoma (PDAC) tissues. Recently a homologue of ACE, angiotensin-converting enzyme 2 (ACE2), was reported to counterbalance the function of ACE, but the expression and role of ACE2 in PDAC are still unclear. In the present study, we analyzed the expression of ACE2 in invasive human PDAC and surrounding non-malignant tissues by Western blot analysis and immunohistochemistry. The ANG II concentration in homogenates of pancreatic tissues was measured with ELISA, and ACE2 protein was detected by Western blot analysis in BxPC3 and SW1990 human pancreatic ductal cancer cells. We have shown for the first time that the expression of ACE2 is decreased in PDAC tissues, in which ANG II was accumulated. Treatment of BxPC3 and SW1990 cells with ANG II decreased the expression of ACE2. Therefore, ANG II may contribute to the down-regulation of ACE2. Moreover, reduction of ACE2 expression by RNA interference promoted the proliferation of cultured pancreatic cancer cells. These findings suggest that ACE2 may have clinical potential as a novel molecular target for the treatment of PDAC.

4
Oncol Rep. 2010 Apr;23(4):941-8.
The angiotensin-converting enzyme 2 in tumor growth and tumor-associated angiogenesis in non-small cell lung cancer
Yun Feng 1 , Huanying Wan, Jialin Liu, Ruifeng Zhang, Qinyun Ma, Bing Han, Yi Xiang, Jiaming Che, Huangming Cao, Xiaochun Fei, Weicheng Qiu
Angiotensin II (AngII) is a multifunctional bioactive peptide and previous studies have shown that the renin-angiotensin system (RAS) of both host and tumor are important in tumor growth and angiogenesis in lung cancer. Angiotensin-converting enzyme 2 (ACE2) is a newly identified component of RAS, with 42% amino acid homology to ACE. However, the expression and function of ACE2 in non-small cell lung cancer (NSCLC) are still unclear. In the present study, we analyzed ACE2 expression in NSCLC tissue by Western blot analysis and immunohistochemistry. AngII concentrations in the tissue homogenate were also detected using radio-immunoassay. We also examined the function of ACE2 by transducing A549 cells with MSCV-ACE2. We have shown for the first time that ACE2 expression decreased in NSCLC tissue in which AngII was higher than the matching non-malignant tissues. A concentration of 10(-6) mol/l of AngII significantly increased expression of vascular endothelial growth factor a (VEGFa) and AT1-R and decreased ACE2 expression. We also found that overexpression of ACE2 may have a protective effect by inhibiting cell growth and VEGFa production in vitro. ACE2 may become a target of novel strategies to treat NSCLC.
Cited by 33 articles

5
Oncol Rep. 2016 Sep;36(3):1403-10.
ACE2 overexpression inhibits acquired platinum resistance-induced tumor angiogenesis in NSCLC
Qijian Cheng 1 , Ling Zhou 1 , Jianping Zhou 1 , Huanying Wan 1 , Qingyun Li 1 , Yun Feng 1
Angiotensin II (AngII) is a multifunctional bioactive peptide in the renin-angiotensin system (RAS). Angiotensin-converting enzyme 2 (ACE2) is a newly identified component of RAS. We previously reported that ACE2 overexpression may inhibit cell growth and vascular endothelial growth factor (VEGF) production in vitro and in vivo. In the present study, we investigated the effect of ACE2 on tumor-associated angiogen-esis after the development of acquired platinum resistance in non-small cell lung cancer (NSCLC). Four NSCLC cell lines, A549, LLC, A549-DDP and LLC-DDP, were used in vitro, while A549 and A549-DDP cells were used in vivo. A549-DDP and LLC-DDP cells were newly established at our institution as acquired platinum-resistant sublines by culturing the former parent cells in cisplatin (CDDP)-containing conditioned medium for 6 months. These platinum-resistant cells showed significantly higher angiotensin II type 1 receptor (AT1R), ACE and VEGF production and lower ACE2 expression than their corresponding parent cells. We showed that ACE2 overexpression inhibited the production of VEGF in vitro and in vivo compared to their corresponding parent cells. We also found that ACE2 overexpression reduced the expression of AT1R and ACE. Additionally, we confirmed that ACE2 overexpres-sion inhibited cell growth and VEGF production while simultaneously suppressing ACE and AT1R expression in human lung cancer xenografts. Our findings indicate that ACE2 overexpression may potentially suppress angiogenesis in NSCLC after the development of acquired platinum resistance.

6
Oncol Rep. 2013 Jun;29(6):2408-14.
doi: 10.3892/or.2013.2370. Epub 2013 Mar 29.
Angiotensin-converting enzyme 2 attenuates the metastasis of non-small cell lung cancer through inhibition of epithelial-mesenchymal transition
Yan-Rong Qian 1 , Yi Guo, Huan-Ying Wan, Liang Fan, Yun Feng, Lei Ni, Yi Xiang, Qing-Yun Li
Angiotensin-converting enzyme 2 (ACE2) is a key enzyme of the renin-angiotensin system (RAS). ACE2 plays a critical counterbalancing role by degrading angiotensin II (Ang II) to Ang 1-7. Recent studies suggest that RAS influences tumor growth and development by its paracrine effects on the tumor microenvironment. Epithelial‑mesenchymal transition (EMT) is now thought to be a process that plays a fundamental role in tumor progression and metastasis. In the present study, we investigated the role of ACE2 in lung cancer metastasis and the mechanism of EMT. This is the first study to elucidate the mechanism through which the overexpression of ACE2 in the A549 lung cancer cell line decreases metastasis formation in vivo and upregulates the expression of E-cadherin both in vitro and in vivo. We also observed the downregulation of vimentin, which supports a role of ACE2 in influencing EMT in lung cancer. Further analysis indicated that ACE2 abrogated the upregulation of TGF-β1-induced EMT markers, such as vimentin and α-smooth muscle actin (αSMA) in vitro in A549 cells. Finally, exposing A549 cells stably expressing ACE2 to DX600, an inhibitor of ACE2, recovered the sensitivity of lung cancer cells to TGF-β1-mediated induction of EMT. Our study demonstrated that ACE2 attenuated the metastasis of lung cancer and may serve as a target for new strategies to inhibit EMT in cancer cells.

7
Comparative Study
Lab Invest. 2007 Feb;87(2):189-98.
Roles for host and tumor angiotensin II type 1 receptor in tumor growth and tumor-associated angiogenesis
Nozomi Imai 1 , Tatsuo Hashimoto, Minoru Kihara, Shin-ichiro Yoshida, Ichiro Kawana, Takuya Yazawa, Hitoshi Kitamura, Satoshi Umemura
Angiotensin II (AII) is a multifunctional bioactive peptide, and host renin-angiotensin system (RAS) is closely associated with tumor growth. Recent reports have described that AII is a proangiogenic growth factor, and that Angiotensin II type 1 (AT1) receptor antagonists reduce tumor growth and tumor-associated angiogenesis. In this paper, we investigated the participation of AT1 receptor-signaling in cancer progression using murine Lewis lung carcinoma (LLC) cells, which express AT1 receptor, and AT1a receptor gene-deficient (AT1a-/-) mice. When LLC cells were implanted subcutaneously into wild-type (WT) mice, developed tumors showed intensive angiogenesis with an induction of vascular endothelial growth factor (VEGF) a. Compared with WT mice, tumor growth and tumor-associated angiogenesis was reduced in AT1a-/- mice with reduced expression of VEGFa. In AT1a-/- mice, administration of the AT1 receptor antagonist, TCV-116, showed further reductions of tumor growth, tumor-associated angiogenesis, and VEGFa expression. In vitro study, the expression of VEGFa mRNA and the production of VEGFa protein in LLC cells were significantly increased by AII, which were cancelled by AT1 receptor antagonist, CV-11974. Although the expression of other angiogenic factors, such as angiopoietin-1, angiopoietin-2, epidermal growth factor, and VEGF receptor 2 mRNA, was also investigated in tumor tissues, the expression of VEGFa was most correlated with tumor size among those other angiogenic factors. VEGFa induction by AT1 receptor-signaling in both host and tumor tissues is one of key regulators of tumor growth and tumor-associated angiogenesis. In conclusion, tumor tissue RAS as well as host tissue RAS were found to have an important role in tumor growth. AT1 receptor-signaling blockade may be a novel and effective target in the treatment of cancer.

SARS-CoV-2 RNA can be reverse-transcribed to be part of chimeric viral-human genome

================================================

CDC: 4,178 Americans DEAD Following Experimental COVID Injections – Deaths from COVID Shots now Equal 20 Years of Recorded Deaths Following Vaccines Since 2001


View: https://rumble.com/vgerov-dr.-sucharit-bhakdi-warns-covid-shots-to-decimate-world-population.html


New Report sheds light on Vaccine Doomsday Cult


View: https://www.bitchute.com/video/cdKu2RXGAWyu/



View: https://www.bitchute.com/video/ecOpzGNqNbgZ/

Thank you. Great response.
 

Birdie

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I have a question. The jabbed people who suffer injury or death are not suffering from a reaction to the virus are they? And it doesn't seem like the people injured by transmission or shedding from a vaccinated/jabbed person are injured by the virus, but something else.

And yet Ray says, "Most people aren’t harmed by the corona virus, so the similar material coming from vaccinated people is likely to be equally harmless."
I'm missing something here.
 

Giraffe

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I have a question. The jabbed people who suffer injury or death are not suffering from a reaction to the virus are they? And it doesn't seem like the people injured by transmission or shedding from a vaccinated/jabbed person are injured by the virus, but something else.

And yet Ray says, "Most people aren’t harmed by the corona virus, so the similar material coming from vaccinated people is likely to be equally harmless."
I'm missing something here.

With a natural infection the spike proteins don't get into your blood stream.
 

Hugh Johnson

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I have a question. The jabbed people who suffer injury or death are not suffering from a reaction to the virus are they? And it doesn't seem like the people injured by transmission or shedding from a vaccinated/jabbed person are injured by the virus, but something else.

And yet Ray says, "Most people aren’t harmed by the corona virus, so the similar material coming from vaccinated people is likely to be equally harmless."
I'm missing something here.
If it's just virus parts, then he right. He probably is. Still, there is a small risk that the vaxx is dangerous to everyone. Prion disease research and those videos about magnets sticking to you after the vaxx suggest that there might be something beyond virus parts there.
 

tankasnowgod

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I have a question. The jabbed people who suffer injury or death are not suffering from a reaction to the virus are they?

What virus? The mRNA shots have no virus in them. This is the biggest difference between them and traditional vaccines.
 

Vileplume

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If it's just virus parts, then he right. He probably is. Still, there is a small risk that the vaxx is dangerous to everyone. Prion disease research and those videos about magnets sticking to you after the vaxx suggest that there might be something beyond virus parts there.
So you're saying the vaccine would cause us to shed virus parts? How would this be possible. Wouldn't vaccinated people shed the mRNA that causes our body to produce the spike protein? In other words, why would they shed the virus materials, rather than the vaccine materials?
 

Birdie

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What virus? The mRNA shots have no virus in them. This is the biggest difference between them and traditional vaccines.
Can you comment on my question? We all know the jab does not contain any type of virus, dead or alive. But look at the quote from Ray that I posted please.

Ray says, "Most people aren’t harmed by the corona virus, so the similar material coming from vaccinated people is likely to be equally harmless."
I'm missing something here.
 

Missenger

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I figured ray meant shedding the spike proteins, the vaccine itself is practically a 'virus' even without viral material. Living around these deranged retards getting vaccinated for prolonged periods of time could ultimately be cancerous for one's health, it's not an issue of getting something moreso than staying in the vicinity of them for an extended period.
 

Birdie

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I've heard people say that Covid preventatives should be used around people who've had the Jab/Shot. But the shot doesn't contain any virus, so why use those preventatives. I am using them but don't think they'll help enough around the vaxed. I think that until we know more I'll limit exposure to "vaccinated" people. Only outdoors or in shopping situations but no indoor visits.
 

tankasnowgod

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Can you comment on my question? We all know the jab does not contain any type of virus, dead or alive. But look at the quote from Ray that I posted please.

Ray says, "Most people aren’t harmed by the corona virus, so the similar material coming from vaccinated people is likely to be equally harmless."
I'm missing something here.

I don't know what, exactly, people would be reacting to. Whether it's the polyethylene glycol, or other novel lipids, or something else in the shot, or the combination. There's a whole lot of proprietary chemicals. Which is a good reason to opt out of this experiment.

Here is the public list of ingredients, by brand-


Something like 2[(polyethylene glycol)-2000]- N,N-ditetradecylacetamide or (4-hydroxybutyl)azanediyl)bis(hexane-6,1-diyl)bis(2-hexyldecanoate) (whatever that is) could cause problems if injected into someone, but I'm not worried about either of those "shedding" from someone who took a shot, for example.

Who knows how well these things are being administered, either. When was the last time you heard about massive groups of people opting for invasive medical procedures at Major League Baseball Stadiums?

Also, the brain geniuses at Pfizer apparently thought it would be a great idea to make pharmacists (or other Temporary Workers) mix the vaccine with diluent before administration, as opposed to just sending out the correct dosage in the first place. Like, they didn't know this was going to be THE most rushed and haphazard administration of (potentially) lethal drugs in history. Maybe they just want to maximize potential errors?

So, some people may be getting an extra strong dose, and reacting to that. Maybe doses haven't been thawed (or stored) properly. Maybe the poor kid they hired off the street with zero medical experience doesn't know where to stick this needle, on top of suffering from cognitive impairment from wearing a mask all day, and is hitting the wrong vein/artery/muscle/ligament/whatever.

You can see handling and mixing instructions here- Product Storage and Dry Ice | CVDvaccine-US.com

Also, some lucky people probably just got saline injections.

The only thing I would think would be a concern (if you aren't swapping bodily fluids with a vaxxed person) would be if that mRNA does, indeed, force their cells to make the spike protein. But I don't know if that's even been demonstrated. If it is, and it becomes a concern, again, I would think the vaxxed person would have symptoms (be they normal cold symptoms or something worse), so you would still have some good real world "warning" signs to keep a distance from such a target.
 
Last edited:

Lollipop2

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The only thing I would think would be a concern (if you aren't swapping bodily fluids with a vaxxed person) would be if that mRNA does, indeed, force their cells to make the spike protein.
This is my thought as well. I have a gut instinct that the fluids are the biggest problem as well as close extended contact like for long hours a days over long periods of time. Just being in a room with someone for a brief period of time doesn’t seem like it will be a big problem.
 

Birdie

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Thank you @tankasnowgod. Overall then, it's looking like if a vaxxed person seems well (is not showing signs of distress) and you are not exchanging body fluids, you could be visiting in a room, without catching something from the vaccine transmission. Okay.
 

Birdie

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I said earlier that my sister in law had the jab. We found out a few days ago that she has had episodes of weakness and heart/lung problem episodes for the past few months and was hospitalized a week ago. She said she had lots of fluid drained out of her in the hospital. Diuretics. Now she says she's had heart episodes with lung involvement/dry cough on and off for the past few months. When asked when she got the shot, she said late February. She sees no connection, saying heart problems run in the family.

She visited with us about two weeks ago. No symptoms of distress at that time.
 

Lollipop2

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I said earlier that my sister in law had the jab. We found out a few days ago that she has had episodes of weakness and heart/lung problem episodes for the past few months and was hospitalized a week ago. She said she had lots of fluid drained out of her in the hospital. Diuretics. Now she says she's had heart episodes with lung involvement/dry cough on and off for the past few months. When asked when she got the shot, she said late February. She sees no connection, saying heart problems run in the family.

She visited with us about two weeks ago. No symptoms of distress at that time.
@Birdie sending good thoughts to your sister in law. This is my concern that the damage shows up later - months if not years. How sad that people don’t recognize the vaccines are the cause. This delays the truth getting around.
 

Birdie

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@Birdie sending good thoughts to your sister in law. This is my concern that the damage shows up later - months if not years. How sad that people don’t recognize the vaccines are the cause. This delays the truth getting around.
Thank you. It's a tragedy. Hard to pinpoint the beginning of her reaction. She said she's had the coughing and heart episodes for months. Sounds like they began shortly after her Feb shot.

But, for sure, we are concerned over long term reactions in people. And, as you say, this clouds perceptions. But the average person is totally sure the shot protects them or at least us! Our a/c guy who is here put back on his mask when he heard we weren't vaxxed. PS we had a dessicated dead rat in our a/c unit.
 

Nighteyes

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Thank you. It's a tragedy. Hard to pinpoint the beginning of her reaction. She said she's had the coughing and heart episodes for months. Sounds like they began shortly after her Feb shot.

But, for sure, we are concerned over long term reactions in people. And, as you say, this clouds perceptions. But the average person is totally sure the shot protects them or at least us! Our a/c guy who is here put back on his mask when he heard we weren't vaxxed. PS we had a dessicated dead rat in our a/c unit.
Oh no poor guy, how did he get in there? ?
 

Birdie

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Oh no poor guy, how did he get in there? ?
Yes poor guy. I don't know but a friend said if the rat can get his head in, then the body will follow. The a/c was making noise and I just assumed something wasn't right and needed repairing. I think it happened during the winter so maybe seeking warmth there.
 

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