Alleen diegenen met ongeschonden bloed zal de vaccin/radiatie holocaust die tegen de mensheid wordt losgelaten overleven ... het spike-eiwit in vaccins veroorzaakt genetische DESINTEGRATIE

Vrijdag 19 november 2021 door: Mike Adams

Tags: badcancer , badhealth , badmedicine , bloed , bloedkanker , bloedcellen , COVID , ontvolking , DNA , uitroeiing , genetische integriteit , genetica , genocide , mRNA , mutaties , NHEJ , pandemie , purebloods , vaccin oorlogen , vaccins

( Natural News ) De podcast van vandaag is als een bom die inslaat en die iedereen moet begrijpen die hoopt de vaccinholocaust te overleven, want het is echt een "genetische bom" tegen de mensheid.

Het vaccin, door het natuurlijke DNA-herstelmechanisme in het lichaam te onderdrukken - bekend als NHEJ of Non-Homologous End Joining - maakt mensen zeer vatbaar voor verwoestende, kankerachtige mutaties, zelfs wanneer ze worden blootgesteld aan zeer lage niveaus van ioniserende straling zoals blootstelling aan zonlicht of mammografie . Nu NHEJ wordt onderdrukt door het spike-eiwit , kan het lichaam het beschadigde DNA niet langer herstellen, en cellen muteren uit de hand, verwoesten het hele lichaam en veroorzaken genetische desintegratie van het organisme.

De studie die dit alles documenteert, werd gepubliceerd in het MDPI-tijdschrift "Viruses" en werd uitgevoerd door wetenschappers van de Universiteit van Stockholm, Zweden:

https://doi.org/10.3390/v13102056

De studie toont aan dat de NHEJ-efficiëntie instort in de aanwezigheid van het mRNA covid-vaccin spike-eiwit:

Geen enkel levend organisme op de planeet kan overleven zonder genetische integriteit . NHEJ maakt deel uit van elke cel in elke levende plant, dier en mens op de planeet.

Het spike-eiwitvaccin is een aanval op de genetische integriteit van mensen, en degenen die het vaccin nemen, zullen grotendeels niet in staat zijn om zich voort te planten omdat hun baby's zichzelf zullen aborteren als gevolg van genetische mutaties . Dit is de reden waarom 82% van de zwangere vrouwen die tijdens hun eerste trimester van de zwangerschap covid-vaccins nemen, hun baby's verliezen door spontane abortussen.

Hoe ontvolkingsglobalisten de mutaties onder de gevaccineerden kunnen versnellen?

Belangrijk is dat, zodra de wezens op een planeet op grote schaal worden geïnjecteerd met het covid-vaccin, globalisten een nucleair ongeval (of nucleair terrorisme) kunnen ontketenen om straling over de planeet te verspreiden. Zelfs een lage blootstelling aan cesium-137 (of strontium-91, jodium-131, enz.) zal een golf van dodelijke kankers ontketenen onder degenen die zijn gevaccineerd. Terwijl normale, gezonde mensen de DNA-schade kunnen herstellen die wordt veroorzaakt door lage niveaus van blootstelling aan ioniserende straling, kunnen gevaccineerde mensen de reparaties nauwelijks uitvoeren (ze hebben ongeveer 90% onderdrukking van DNA-herstel).

Zo zullen de kankercijfers onder de gevaccineerden omhoogschieten, en wanneer ze sterven, kunnen de sterfgevallen worden toegeschreven aan kanker in plaats van aan de vaccins. Dus deze binaire wapenregeling stelt vaccin-pooiers ook in staat om de schuld voor de vaccins te ontlopen. Het verdoezelt sterfgevallen door vaccins door ze te categoriseren als sterfgevallen door kanker.

Het enige wat ze nodig hebben is nog een Tsjernobyl-, Fukushima- of nucleaire explosie ergens op het noordelijk halfrond - bijna overal - en de wind zal de radio-isotopen over de halve planeet verspreiden, en de lage niveaus van ioniserende straling bereiken die nodig zijn om gevaccineerde mensen om te zetten in door kanker geteisterde mutanten met versnelde sterfgevallen.

Het is zeer onwaarschijnlijk dat de gevaccineerde personen die niet door de kankers worden gedood, levensvatbare nakomelingen kunnen produceren vanwege DNA-beschadiging van sperma en eicellen.

Interessant is dat als het eenmaal duidelijk wordt dat gevaccineerde individuen geen zonlicht kunnen verdragen zonder genetische mutaties, ze het daglicht zullen mijden en nachtdieren zullen worden .

In culturele mythen zijn vampiers nachtdieren die onmiddellijk uiteenvallen wanneer zonlicht hun huid raakt. In werkelijkheid zal de desintegratie veel meer tijd kosten, maar het is een soortgelijk idee:

Covid-vaccins + zonlicht = genetische desintegratie .

Alleen volbloeden zullen zich kunnen voortplanten, dus de toekomst van de mensheid behoort toe aan degenen die mRNA-vaccins afwijzen

Degenen die covid-vaccins afwijzen, staan ​​​​bekend als 'zuivere bloeden'. Zij zijn de enigen die in staat zullen zijn de genetische integriteit voor de komende generaties te behouden, wat betekent dat de toekomst van de mensheid toebehoort aan degenen die covid-vaccins afwijzen . (Mensen die spike-eiwit / mRNA-covid-opnamen maken, winnen de Darwin Award ...)

Volgens God is via het Oude Testament het bloed waar het leven bestaat. Je lichaam maakt elke minuut twee miljoen rode bloedcellen aan en deze worden in je botten gemaakt. Dit is de reden waarom Genesis zegt dat Eva werd gemaakt uit de rib van Adam. De botten zijn waar het DNA bestaat om bloed te produceren, de essentie van het leven, en om het genetische patroon te vinden dat de biologie van een nieuw wezen beschrijft.

Een persoon die aan genetische mutaties in het bloed lijdt, wordt gediagnosticeerd met leukemie , in wezen bloedkanker. Dit is een desintegratie van de genetische integriteit van hun bloedproductietemplates, simpel gezegd, en geen enkel zoogdier is levensvatbaar op de lange termijn wanneer de genetische integriteit van hun bloed wordt vernietigd.

Toch is dit precies wat de vaccins zullen bereiken wanneer ze gepaard gaan met blootstelling aan lage ioniserende straling. Nogmaals vermeld:

Spike-eiwitten + Ioniserende straling = DNA-mutaties / verlies van genetische integriteit

Degenen die de spike-eiwitinjecties namen, ervaren al een versnelde groei van kankertumoren. Dit wordt breed uitgemeten onder natuurgeneeskundige artsen en analisten. Hoewel het mogelijk is dat DNA-mutaties een halt worden toegeroepen door een agressief voedingsontgiftingsprogramma en een levenslange levensstijl tegen kanker, leiden de meeste mensen in feite een pro-kankerlevensstijl via hun giftige voeding, giftige producten voor persoonlijke verzorging en giftige woonomgevingen binnenshuis. . De meeste mensen hebben bovendien een vitamine D-tekort, wat betekent dat ze in wezen "kankerfabrieken" zijn, zelfs voordat er spike-eiwitinjecties kwamen.

Zo zijn we op het punt om een explosie in kanker wereldwijd te zien als gevolg van covid vaccins. Dit zal echt versnellen in 2022, en we zullen in 2022 gemakkelijk meer dan een miljoen sterfgevallen door kanker in de VS zien (hoewel de gegevens hoogstwaarschijnlijk pas in 2024 beschikbaar zullen zijn). In de komende tien jaar (2022 – 2032) zullen we waarschijnlijk tientallen miljoenen sterfgevallen door kanker zien in de Verenigde Staten.

Elke vrijgave van straling door globalisten zal deze aantallen alleen maar versnellen en meer levens kosten. (Dat is het doel van de globalisten.)

Ondertussen zullen degenen die de mRNA-spike-eiwitinjecties namen, gemuteerde baby's baren die geen genetische levensvatbaarheid hebben, zelfs als ze hun eigen mutaties overleven. Momenteel heeft ongeveer de helft van de menselijke bevolking covid-prikken van een of andere soort genomen, wat betekent dat de ontvolkingsglobalisten hun doel om de vruchtbaarheid / genetische levensvatbaarheid voor een aanzienlijk deel van het menselijk ras te vernietigen, al hebben bereikt.

Het afsterven is nu begonnen. Deze winter zal het aantal sterfgevallen door kanker in heel Amerika exploderen, en het komende decennium zullen ze omhoogschieten bij degenen die goedgelovig genoeg waren om te worden geïnjecteerd met dodelijke biowapens met spike-eiwitten. Maak je klaar om een ​​vloedgolf van kankers te zien in Amerika, Europa, Australië, Canada en elk ander land waar goedgelovige mensen zelfmoord hebben gepleegd door vaccins.

Ik behandel het volledige, verbazingwekkende verhaal van dit alles in de Situation Update-podcast van vandaag:

Brighteon.com/fef16093-6fd9-43a1-a5cb-cdecb4c63e64

Vind elke dag een nieuwe podcast (samen met krachtige interviews en ander commentaar) op het Health Ranger Report-kanaal op Brighteon.com:

https://www.brighteon.com/channels/hrreport

 

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Open Access Article

SARS–CoV–2 Spike Impairs DNA Damage Repair and Inhibits V(D)J Recombination In Vitro

https://www.mdpi.com/1999-4915/13/10/2056/htm

by 

Hui Jiang

 ^1,2,* and

Ya-Fang Mei

 ^2,*

¹  Department of Molecular Biosciences, The Wenner–Gren Institute, Stockholm University, SE-10691 Stockholm, Sweden

²  Department of Clinical Microbiology, Virology, Umeå University, SE-90185 Umeå, Sweden

^*  Authors to whom correspondence should be addressed.

Academic Editor: Oliver Schildgen

Viruses 2021, 13(10), 2056; https://doi.org/10.3390/v13102056

Received: 20 August 2021 / Revised: 8 September 2021 / Accepted: 8 October 2021 / Published: 13 October 2021

(This article belongs to the Special Issue SARS-CoV-2 Host Cell Interactions)

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS–CoV–2) has led to the coronavirus disease 2019 (COVID–19) pandemic, severely affecting public health and the global economy. Adaptive immunity plays a crucial role in fighting against SARS–CoV–2 infection and directly influences the clinical outcomes of patients. Clinical studies have indicated that patients with severe COVID–19 exhibit delayed and weak adaptive immune responses; however, the mechanism by which SARS–CoV–2 impedes adaptive immunity remains unclear. Here, by using an in vitro cell line, we report that the SARS–CoV–2 spike protein significantly inhibits DNA damage repair, which is required for effective V(D)J recombination in adaptive immunity. Mechanistically, we found that the spike protein localizes in the nucleus and inhibits DNA damage repair by impeding key DNA repair protein BRCA1 and 53BP1 recruitment to the damage site. Our findings reveal a potential molecular mechanism by which the spike protein might impede adaptive immunity and underscore the potential side effects of full-length spike-based vaccines.

Keywords: SARS–CoV–2; spike; DNA damage repair; V(D)J recombination; vaccine                                      

1. Introduction

2. Materials and Methods

            2.1. Antibodies and Reagents

2.2. Plasmids

2.3. Cells and Cell Culture

2.4. HR and NHEJ Reporter Assays

2.5. Cellular Fractionation and Immunoblotting

2.6. Comet Assay

2.7. Immunofluorescence

2.8. Analysis of V(D)J Recombination

2.9. Statistical Analysis

3. Results

3.1. Effect of Nuclear–Localized SARS–CoV–2 Viral Proteins on DNA Damage Repair

 DNA damage repair occurs mainly in the nucleus to ensure genome stability. Although SARS–CoV–2 proteins are synthesized in the cytosol [1], some viral proteins are also detectable in the nucleus, including Nsp1, Nsp5, Nsp9, Nsp13, Nsp14, and Nsp16 [19]. We investigated whether these nuclear-localized SARS–CoV–2 proteins affect the host cell DNA damage repair system. For this, we constructed these viral protein expression plasmids together with spike and nucleoprotein expression plasmids, which are generally considered cytosol–localized proteins. We confirmed their expression and localization by immunoblotting and immunofluorescence (Figure 1A and Figure S1A). Our results were consistent with those from previous studies [19]; Nsp1, Nsp5, Nsp9, Nsp13, Nsp14, and Nsp16 proteins are indeed localized in the nucleus, and nucleoproteins are mainly localized in the cytosol. Surprisingly, we found the abundance of the spike protein in the nucleus (Figure 1A). NHEJ repair and homologous recombination (HR) repair are two major DNA repair pathways that not only continuously monitor and ensure genome integrity but are also vital for adaptive immune cell functions [9]. To evaluate whether these viral proteins impede the DSB repair pathway, we examined the repair of a site-specific DSB induced by the I–SceI endonuclease using the direct repeat–green fluorescence protein (DR–GFP) and the total-NHEJ-GFP (EJ5–GFP) reporter systems for HR and NHEJ, respectively [15,16]. Overexpression of Nsp1, Nsp5, Nsp13, Nsp14, and spike proteins diminished the efficiencies of both HR and NHEJ repair (Figure 1B–E and Figure S2A,B). Moreover, we also found that Nsp1, Nsp5, Nsp13, and Nsp14 overexpression dramatically suppressed proliferation compared with other studied proteins (Figure S3A,B). Therefore, the inhibitory effect of Nsp1, Nsp5, Nsp13, and Nsp14 on DNA damage repair may be due to secondary effects, such as growth arrest and cell death. Interestingly, overexpressed spike protein did not affect cell morphology or proliferation but significantly suppressed both HR and NHEJ repair (Figure 1B–E, Figures S2A,B and S3A,B).

Figure 1. Effect of severe acute respiratory syndrome coronavirus 2 (SARS–CoV–2) nuclear-localized proteins on DNA damage repair. (A) Subcellular distribution of the SARS–CoV–2 proteins. Immunofluorescence was performed at 24 h after transfection of the plasmid expressing the viral proteins into HEK293T cells. Scale bar: 10 µm. (B) Schematic of the EJ5-GFP reporter used to monitor non-homologous end joining (NHEJ). (C) Effect of empty vector (E.V) and SARS–CoV–2 proteins on NHEJ DNA repair. The values represent the mean ± standard deviation (SD) from three independent experiments (see representative FACS plots in Figure S2A). (D) Schematic of the DR-GFP reporter used to monitor homologous recombination (HR). (E) Effect of E.V and SARS–CoV–2 proteins on HR DNA repair. The values represent the mean ± SD from three independent experiments (see representative FACS plots in Figure S2B). The values represent the mean ± SD, n = 3. Statistical significance was determined using one-way analysis of variance (ANOVA) in (C,E). ** p < 0.01, *** p < 0.001, **** p <  0.0001.

3.2. SARS–CoV–2 Spike Protein Inhibits DNA Damage Repair

Because spike proteins are critical for mediating viral entry into host cells and are the focus of most vaccine strategies [20,21], we further investigated the role of spike proteins in DNA damage repair and its associated V(D)J recombination. Spike proteins are usually thought to be synthesized on the rough endoplasmic reticulum (ER) [1]. After posttranslational modifications such as glycosylation, spike proteins traffic via the cellular membrane apparatus together with other viral proteins to form the mature virion [1]. Spike protein contains two major subunits, S1 and S2, as well as several functional domains or repeats [22] (Figure 2A). In the native state, spike proteins exist as inactive full–length proteins. During viral infection, host cell proteases such as furin protease activate the S protein by cleaving it into S1 and S2 subunits, which is necessary for viral entry into the target cell [23]. We further explored different subunits of the spike protein to elucidate the functional features required for DNA repair inhibition. Only the full–length spike protein strongly inhibited both NHEJ and HR repair (Figure 2B–E and Figure S4A,B). Next, we sought to determine whether the spike protein directly contributes to genomic instability by inhibiting DSB repair. We monitored the levels of DSBs using comet assays. Following different DNA damage treatments, such as γ–irradiation, doxorubicin treatment, and H₂O₂ treatment, there is less repair in the presence of the spike protein (Figure 2F,G). Together, these data demonstrate that the spike protein directly affects DNA repair in the nucleus.

Figure 2. Severe acute respiratory syndrome coronavirus 2 (SARS–CoV–2) spike protein inhibits DNA damage repair. (A) Schematic of the primary structure of the SARS–CoV–2 spike protein. The S1 subunit includes an N–terminal domain (NTD, 14–305 residues) and a receptor–binding domain (RBD, 319–541 residues). The S2 subunit consists of the fusion peptide (FP, 788–806 residues), heptapeptide repeat sequence 1 (HR1, 912–984 residues), HR2 (1163–1213 residues), TM domain (TM, 1213–1237 residues), and cytoplasm domain (CT,1237–1273 residues). (B,C) Effect of titrated expression of the spike protein on DNA repair in HEK–293T cells. (D,E) Only full-length spike protein inhibits non-homologous end joining (NHEJ) and homologous recombination (HR) DNA repair. The values represent the mean ± SD from three independent experiments (see representative FACS plots in Figure S4A,B). (F) Full–length spike (S–FL) protein–transfected HEK293T cells exhibited more DNA damage than empty vector-, S1–, and S2–transfected cells under different DNA damage conditions. For doxorubicin: 4 µg/mL, 2 h. For γ–irradiation: 10 Gy, 30 min. For H₂O₂: 100 µM, 1 h. Scale bar: 50 µm. (G) Corresponding quantification of the comet tail moments from 20 different fields with n > 200 comets of three independent experiments. Statistical significance was assessed using a two-way analysis of variance (ANOVA). NS (Not Significant): * p > 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

3.3. Spike Proteins Impede the Recruitment of DNA Damage Repair Checkpoint Proteins

To confirm the existence of spike protein in the nucleus, we performed subcellular fraction analysis and found that spike proteins are not only enriched in the cellular membrane fraction but are also abundant in the nuclear fraction, with detectable expression even in the chromatin–bound fraction (Figure 3A). We also observed that the spike has three different forms, the higher band is a highly glycosylated spike, the middle one is a full–length spike, and the lower one is a cleaved spike subunit. Consistent with the comet assay, we also found the upregulation of the DNA damage marker, γ–H2A.X, in spike protein–overexpressed cells under DNA damage conditions (Figure 3B). A recent study suggested that spike proteins induce ER stress and ER–associated protein degradation [24]. To exclude the possibility that the spike protein inhibits DNA repair by promoting DNA repair protein degradation, we checked the expression of some essential DNA repair proteins in NHEJ and HR repair pathways and found that these DNA repair proteins were stable after spike protein overexpression (Figure 3C). To determine how the spike protein inhibits both NHEJ and HR repair pathways, we analyzed the recruitment of BRCA1 and 53BP1, which are the key checkpoint proteins for HR and NHEJ repair, respectively. We found that the spike protein markedly inhibited both BRCA1 and 53BP1 foci formation (Figure 3D–G). Together, these data show that the SARS–CoV–2 full–length spike protein inhibits DNA damage repair by hindering DNA repair protein recruitment.

Figure 3. Severe acute respiratory syndrome coronavirus 2 (SARS–CoV–2) spike protein impedes the recruitment of DNA damage repair checkpoint proteins. (A) Membrane fraction (MF), cytosolic fraction (CF), soluble nuclear fraction (SNF), and chromatin-bound fraction (CBF) from HEK293T cells transfected with SARS–CoV–2 spike protein were immunoblotted for His-tag spike and indicated proteins. (B) Left: Immunoblots of DNA damage marker γH2AX in empty vector (E.V)– and spike protein–expressing HEK293T cells after 10 Gy γ-irradiation. Right: corresponding quantification of immunoblots in left. The values represent the mean ± SD (n = 3). Statistical significance was determined using Student’s t-test. **** p < 0.0001. (C) Immunoblots of DNA damage repair related proteins in spike protein–expressing HEK293T cells. (D) Representative images of 53BP1 foci formation in E.V– and spike protein-expressing HEK293 cells exposed to 10 Gy γ–irradiation. Scale bar: 10 µm. (E) Quantitative analysis of 53BP1 foci per nucleus. The values represent the mean ± SEM, n = 50. (F) BRCA1 foci formation in empty vector- and spike protein-expressing HEK293 cells exposed to 10 Gy γ–irradiation. Scale bar: 10 µm. (G). Quantitative analysis of BRCA1 foci per nucleus. The values represent the mean ± SEM, n = 50. Statistical significance was determined using Student’s t-test. **** p < 0.0001.

3.4. Spike Protein Impairs V(D)J Recombination In vitro

DNA damage repair, especially NHEJ repair, is essential for V(D)J recombination, which lies at the core of B and T cell immunity [9]. To date, many approved SARS–CoV–2 vaccines, such as mRNA vaccines and adenovirus–COVID–19 vaccines, have been developed based on the full–length spike protein [25]. Although it is debatable whether SARS–CoV–2 directly infects lymphocyte precursors [26,27], some reports have shown that infected cells secrete exosomes that can deliver SARS–CoV–2 RNA or protein to target cells [28,29]. We further tested whether the spike protein reduced NHEJ–mediated V(D)J recombination. For this, we designed an in vitro V(D)J recombination reporter system according to a previous study [18] (Figure S5). Compared with the empty vector, spike protein overexpression inhibited RAG–mediated V(D)J recombination in this in vitro reporter system (Figure 4).

Figure 4. Spike protein impairs V(D)J recombination in vitro. (A) Schematic of the V(D)J reporter system. (B) Representative plots of flow cytometry show that the SARS–CoV–2 spike protein impedes V(D)J recombination in vitro. (C) Quantitative analysis of relative V(D)J recombination. The values represent the mean ± SD, n = 3. Statistical significance was determined using Student’s t-test. **** p < 0.0001.

4. Discussion

Our findings provide evidence of the spike protein hijacking the DNA damage repair machinery and adaptive immune machinery in vitro. We propose a potential mechanism by which spike proteins may impair adaptive immunity by inhibiting DNA damage repair. Although no evidence has been published that SARS–CoV–2 can infect thymocytes or bone marrow lymphoid cells, our in vitro V(D)J reporter assay shows that the spike protein intensely impeded V(D)J recombination. Consistent with our results, clinical observations also show that the risk of severe illness or death with COVID–19 increases with age, especially older adults who are at the highest risk [22]. This may be because SARS–CoV–2 spike proteins can weaken the DNA repair system of older people and consequently impede V(D)J recombination and adaptive immunity. In contrast, our data provide valuable details on the involvement of spike protein subunits in DNA damage repair, indicating that full–length spike–based vaccines may inhibit the recombination of V(D)J in B cells, which is also consistent with a recent study that a full–length spike–based vaccine induced lower antibody titers compared to the RBD–based vaccine [28]. This suggests that the use of antigenic epitopes of the spike as a SARS–CoV–2 vaccine might be safer and more efficacious than the full–length spike. Taken together, we identified one of the potentially important mechanisms of SARS–CoV–2 suppression of the host adaptive immune machinery. Furthermore, our findings also imply a potential side effect of the full–length spike–based vaccine. This work will improve the understanding of COVID–19 pathogenesis and provide new strategies for designing more efficient and safer vaccines.

Supplementary Materials

The following are available online at https://www.mdpi.com/article/10.3390/v13102056/s1, Figure S1: Expression of nuclear–localized SARS–CoV–2 proteins in human cells, Figure S2: Effect of nuclear SARS–CoV–2 proteins on NHEJ– and HR–DNA repair pathway, Figure S3: Nsp1, Nsp5, Nsp13, Nsp14 but not spike inhibit cell proliferation, Figure S4: Effect of SARS–CoV–2 spike mutants on NHEJ– and HR– DNA repair pathway, Figure S5: In vitro V(D)J recombination assay.

Author Contributions

H.J. conceived and designed the study. H.J. and Y.-F.M. supervised the study, performed experiments, and interpreted the data. Writing—original draft preparation, H.J.; Writing—review and editing, H.J. and Y.-F.M.; funding acquisition, Y.-F.M. All authors have read and agreed to the published version of the manuscript.

Funding

This work was supported by Umeå University, Medical Faculty’s Planning grants for COVID–19 (research project number: 3453 16032 to Y.F.M.); the Lion’s Cancer Research Foundation at Umeå University (grants: LP 17–2153, AMP 19–982, and LP 20–2256 to Y.F.M.), and the base unit’s ALF funds for research at academic healthcare units and university healthcare units in the northern healthcare region (ALF–Basenheten: 2019, 2020, 2021 to Y.F.M.).

Institutional Review Board Statement

Not applicable, because of this study not involving humans or animals.

Informed Consent Statement

Not applicable, because of this study not involving humans.

Data Availability Statement

The data presented in this study are available in the main text and Supplementary Materials.

Conflicts of Interest

The authors have declared that no competing interests exist. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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