“During the conference she showed codes on the bottles where each contains 1, 2 or 3 digits, and then explained the meaning of those numbers.
Number 1 is the placebo, saline. Number 2 is a the mRNA. The number 3 is an mRNA stick that contains the onco gene, linked to the adenovirus that contributes to the development of cancer. She said those receiving the number 3 bottle will develop soft tissue cancer within two years of receiving the jab.”
So she secretly gave the politicians number 3? By ‘accident’, of course.
“If you check hard enough, you will find references to that fact that certain batches of vaccine deployed in the USA have far more deadly consequences than others. Deaths and bad reactions are not occurring randomly as one might expect, they are in clusters where the vaccine batch is the common denominator. Other batches have essentially no consequences. What is in them? Enquiring minds want to know.”
People are referencing a Robert O Young.
And in the UK, Amazon and other companies are tracking you like a prisoner:
The Daily Record reports, “We have learned the NHS mobile phone app which presents the personal medical information in the form of a QR Code shares data with companies including Amazon, Microsoft, ServiceNow, Royal Mail and an AI facial recognition firm.”
Cardiac issues paper:
Abstract 10712: Mrna COVID Vaccines Dramatically Increase Endothelial Inflammatory Markers and ACS Risk as Measured by the PULS Cardiac Test: a Warning
RE ONCO GENES, TEXTBOOK:
“Infection may be productive, abortive, or latent. In productive infections, the viral genome is transcribed in the nucleus, mRNA is translated in the cytoplasm, and virions self-assemble in the nucleus. In latent infections and in transformed and tumor cells, viral DNA is integrated into the host genome. Virus-host DNA recombinants are also found in productive infections.”
“Most adolescents and adults have circulating neutralizing antibodies; immunity is widespread. Cytotoxic T lymphocytes destroy adenovirus-infected cells.
There is no treatment. Whole-virus vaccines are not used because of the potential risk of oncogenesis. Other vaccines, including recombinant vaccines, are under development, but adenoviruses do not represent a serious health hazard.”
“Host cells differ in permissivity for adenovirus types (Table 67-2). In permissive cells, the virus multiplies productively and kills the host cell. Other cells are semipermissive, allowing replication at low efficiency, whereas in still others replication is blocked and the infection is abortive. As discussed below, in some abortive infections all or part of the genome may be integrated into the host DNA, resulting in a latent infection, which may lead to oncogenic transformation.”
“Most of the adenovirus genes (Fig. 67-3) are transcribed by the host DNA-dependent RNA polymerase II in a complex transcriptional program. This program is regulated by the nucleotide sequences and the structure of the viral promoters and by a host of cell-encoded transcription factors that recognize specific upstream and downstream nucleotide sequence motifs in the promoters. Genes in the E1A region of the adenovirus genome are the first to be transcribed. One protein product of this gene region is a transactivator that is essential for the activation of all other viral genes. This immediate-early viral function can also activate or inactivate certain cellular genes.”
“Virus interaction with a host cell can be blocked at many different steps, thus leading to an incomplete or abortive cycle. Depending on the permissivity of the host cell, different types of adenovirus-host cell interactions can be distinguished (Table 67-2). Many cultured human epithelioid cell lines are productively infected by human adenoviruses. Rat cells are semipermissive (e.g., for Ad5), and permit viral replication only at low efficiency. The outcome of an adenovirus infection depends on the animal species, cell type, and virus type involved. For example, hamster cells are abortively infected with human Ad12. The viral DNA is transported to the nucleus, where part of it is integrated into the host cell genome. Both in productively and in abortively-infected cells, the viral DNA gravitates towards and becomes transiently associated with the host cell chromosomes as demonstrated by fluorescent in situ hybridization. Most of the early viral genes are transcribed, but the late genes remain silent in the host cells. Ad12 DNA replication in hamster cells cannot be detected with the most sensitive techniques. The major late promoter of Ad12 DNA is inactive in both uninfected and Ad12-infected hamster cells, whereas it functions in infected human cells. Ad2 cannot replicate in monkey cells; in this case, the translation of some of the late viral mRNAs is amiss. The adenovirus genome persists, perhaps for a very long time, in cells of the human tonsils. It is not known how adenovirus replication in this human organ is restricted.”
“Latency and persistence of, as well as oncogenicity by, DNA viruses are frequently associated with integration of all or part of the viral genome into the host cell DNA. Integration of adenovirus DNA has been demonstrated in abortively infected cells, in adenovirus-transformed cells, and in Ad12-induced tumor cells. In productively infected human cells, recombination between adenovirus DNA and host cell DNA has also been observed. However, it is not known whether this recombination can lead to stable integration, because in the productive infection cycle the host cells are eventually killed. There is evidence that early in productively infected human cells Ad12 DNA becomes preferentially integrated into human chromosome 1.“
GM humans, no longer human beings legally.
They’re signing you.
“Recently, an interesting alternate mechanism of insertional mutagenesis in adenovirus-transformed or Ad12-induced tumor cells was discovered. Insertion of Ad12, plasmid or bacteriophage lambda DNA into established mammalian genomes can lead to extensive changes in patterns of cellular DNA methylation far away from and on chromosomes different from those of the site of viral DNA integration. Since patterns of DNA methylation are related to expression patterns and genome organization, alterations in patterns of DNA methylation might affect many cellular functions whose altered expression may play a role in insertional mutagenesis and viral oncogenesis.”
“Analyses of several different integration sites in transformed cell lines suggest that transcriptionally active regions of the host cellular genome, which have a characteristic chromatin structure, are most apt to recombine with foreign (viral) DNA. Adenovirus DNA frequently recombines with cellular DNA via its termini, and terminal viral nucleotides are often deleted from the integrated viral DNA molecule. In general, considerable variability is observed in the structure of the site of integration. No specific cellular DNA sequence has been found at the site of viral DNA insertion in established cell lines. Cellular DNA can be deleted at the insertion site, or the cellular site can be preserved to the last nucleotide. Ad12 DNA is frequently integrated nearly intact in the DNA of nonpermissive hamster cells. However, Ad2 DNA is usually integrated in fragments in hamster cells permissive for Ad2.”
“The adenovirus system has also served as a model for studying the function of sequence-specific promoter methylations in mammalian cells. Upon integration of the adenovirus genome into the host cell genome, a highly specific pattern of methylation is de novo imposed on the integrated viral genome during many cell generations. This de novo methylation is not primarily dependent on nucleotide sequence. Site of integration, structure of integrate and genetics of the host cell are contributing factors. There is evidence from analyses in many different biologic systems that sequence-specific promoter methylations can cause long-term gene inactivation.”
Why so many boosters?
“Ad12-transformed hamster cells or Ad12-induced hamster tumor cells maintained in culture can eventually lose the integrated copies of viral DNA. This loss suggests that adenoviruses might cause transformation by a “hit and run” mechanism.”
“The so-called oncogenes represent a set of cellular genes that are involved in many different ways in growth control. Oncogenes in adenovirus-induced tumor or transformed cells have received surprisingly little attention. The few studies on this topic have reported occasional changes of oncogene activity, particularly for the myc gene. Moreover, E1 proteins can bind tightly to the product of the retinoblastoma (RB) or the p53 gene, which are considered to be anti-oncogenes. It has been suggested that the fixation of the anti-oncogene products by E1 proteins might contribute to the transformation of cells. The interplay of several viral and cellular factors may eventually alter the cellular growth control and weaken or overcome the host defenses in such a way that an adenovirus-transformed rodent cell can grow into a solid tumor.”
Little attention? Wanna bet?
“Since many human tumors do not contain even traces of adenovirus genes or gene products, the possibility that adenoviruses cause human tumors is low. New, more sensitive techniques are now available. Moreover, the “hit and run” hypothesis has not been ruled out. Since even experimentally induced tumors can lose the viral genome and retain oncogenicity, this possible mechanism of transformation of human cells is still being studied.”
NOT known to what extent they “continue to replicate” through life.
“Adenoviruses have been isolated from severely immunocompromised patients, such as those with acquired immune deficiency syndrome (AIDS). Many of these isolates, including the adenovirus types 42 to 47, are found in the urine of AIDS patients.”
“Since adenoviruses are excellent antigens, vaccination could be very effective. However, viral vaccines usually have not been used because adenoviruses are involved in tumorigenesis in animals and in cell culture. Moreover, adenovirus infections only rarely cause serious complications. Nevertheless, efforts are under way to produce vaccines by recombinant DNA technology. Purified hexon or fiber preparations induce high levels of neutralizing antibodies, and vaccines based on these proteins have been tested successfully.”
“Adenoviruses have been used as vector systems in approaches towards human somatic gene therapy. The early region E3 of the viral genome is not essential for viral replication in cell culture and can be removed to yield space in the genome for the insertion of foreign genes constructed for therapeutic purposes. Moreover, the E1 region of the adenoviral genome can be excised to incapacitate viral replication in human tissues thus offering further space for foreign gene insertions. Manipulated, E1-deficient adenovirions can be propagated in the human cell line 293 which contains in an integrated form and constitutively expresses the E1 region of Ad5. Results adduced to date indicate that manipulated adenoviral genomes, e.g. with the test gene for β-galactosidase under eukaryotic promoter control inserted, persist and continue to express this test gene in different organs of rodents for periods up to months. It is not known whether these viral genomes can integrate into the host genome under these conditions.”
Extensive studies on viral-mediated oncogenic transformation by human adenoviruses have revealed much of our current understanding on the molecular mechanisms that are involved in the process. To date, these studies have shown that cell transformation is a multistep process regulated by the cooperation of several adenoviral gene products encoded in the early regions 1 (E1) and 4 (E4). Early region 1A immortalizes primary rodent cells, whereas co-expression of early region protein 1B induces full manifestation of the transformed phenotype. Beside E1 proteins, also some E4 proteins have partial transforming activities through regulating many cellular pathways. Here, we summarize recent data of how adenoviral oncoproteins may contribute to viral transformation and discuss the challenge of pinpointing the underlying mechanisms.
2001 breast cancer
A coronavirus vaccine known as ChAdOx1 nCoV-19 or AZD1222 was developed by the University of Oxford and AstraZeneca to treat severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (the cause of COVID-19). In this vaccine, a modified version of a chimpanzee adenovirus (ChAdOx1) is used which can enter human cells but not replicate inside. A gene for the coronavirus vaccine was added into the adenovirus DNA, allowing the vaccine to target the spike proteins that SARS-CoV-2 uses to enter human cells.
Use of adenovirus type-5 vectored vaccines: a cautionary tale
We are writing to express concern about the use of a recombinant adenovirus type-5 (Ad5) vector for a COVID-19 phase 1 vaccine study,1 and subsequent advanced trials.
Over a decade ago, we completed the Step and Phambili phase 2b studies that evaluated an Ad5 vectored HIV-1 vaccine administered in three immunisations for efficacy against HIV-1 acquisition.2, 3 Both international studies found an increased risk of HIV-1 acquisition among vaccinated men.2, 4 The Step trial found that men who were Ad5 seropositive and uncircumcised on entry into the trial were at elevated risk of HIV-1 acquisition during the first 18 months of follow-up.5 The hazard ratios were particularly high among men who were uncircumcised and Ad5 seropositive, and who reported unprotected insertive anal sex with a partner who was HIV-1 seropositive or had unknown serostatus at baseline, suggesting the potential for increased risk of penile acquisition of HIV-1. Importantly for considering the potential use of Ad5 vectors for COVID-19 infection, a similar increased risk of HIV infection was also observed in heterosexual men who enrolled in the Phambili study.4 This effect appeared to persist over time. Both studies involved an Ad5 construct that did not have the HIV-1 envelope. In another HIV study, done only in men who were Ad5 seronegative and circumcised, a DNA prime followed by an Ad5 vector were used, in which both constructs contained the HIV-1 envelope.6 No increased risk of HIV infection was noted. A consensus conference about Ad5 vectors held in 2013 and sponsored by the National Institutes of Health indicated the most probable explanation for these differences related to the potential counterbalancing effects of envelope immune responses in mitigating the effects of the Ad5 vector on HIV-1 acquisition.7 The conclusion of this consensus conference warned that non-HIV vaccine trials that used similar vectors in areas of high HIV prevalence could lead to an increased risk of HIV-1 acquisition in the vaccinated population. The increased risk of HIV-1 acquisition appeared to be limited to men; a similar increase in risk was not seen in women in the Phambili trial.4
Regulation of the cell cycle and apoptosis by the oncogenes of adenovirus
The oncogenes of adenovirus, E1A and E1B, play an essential role in establishing a productive virus infection in human cells, and are both necessary and sufficient for transformation of primary rodent epithelial cells (White, 1995, 1998). The products of the E1A and E1B genes also modulate the interaction between the infected cell and the immune system of the human or rodent host (Wold et al., 1999). E1A stimulates entry into S phase to create the appropriate environment for the replication of viral DNA in productively infected human cells. This same growth deregulatory function of E1A is also essential to the transformation of primary rodent cells. E1A accomplishes cell cycle deregulation by binding to and perturbing the normal function of key negative regulators of cell growth, including the retinoblastoma protein (Rb), and the transcriptional coactivator p300. Ironically, these very activities of E1A that are required for productive virus infection and oncogenic transformation also stimulate programmed cell death (apoptosis) (White, 1995, 1998). Apoptosis is the cellular defensive response to gross perturbation in cell growth regulation induced by E1A during virus infection and transformation. E1A expression in productively infected cells also decreases the threshold of killing by death signaling cytokines, such as tumor necrosis factor-alpha (TNF-α), which facilitates death of infected cells. Neither of these events is favorable for virus production. In transformation, the induction of apoptosis by E1A nearly abrogates the oncogenic activity of E1A, and necessitates that E1A be coexpressed with an inhibitor of apoptosis for transformation to occur. All of these pro-apoptotic activities are counteracted by expression of E1B, which sustains productive infection and transformation.
You get the picture.