Mutated virus resistant to human antibodies?

Geo

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I feel that i need to post this and any ideas are welcome. There is a doctor in Greece an oncologist with excellent credentials Dr. Dimitrios Antoniou Phd, FRCS who claims that all the mutations come from the vaccine and that the mutated virus has developped resistance to human antibodies, just like microbes after treatment with antibiotics.
Another very suspicious item of news is the agreement of greek PM , a fanatical promoter of vaccination, with the Israeli PM to produce together an inhaled medicine for curing COVID 19. I will never believe that these people plan something good for the people. Sorry for the Greek but that is all it says.
 

tankasnowgod

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I feel that i need to post this and any ideas are welcome. There is a doctor in Greece an oncologist with excellent credentials Dr. Dimitrios Antoniou Phd, FRCS who claims that all the mutations come from the vaccine and that the mutated virus has developped resistance to human antibodies, just like microbes after treatment with antibiotics.
Another very suspicious item of news is the agreement of greek PM , a fanatical promoter of vaccination, with the Israeli PM to produce together an inhaled medicine for curing COVID 19. I will never believe that these people plan something good for the people. Sorry for the Greek but that is all it says.

I personally don't buy the idea that antibiotics themselves cause "Antibiotic Resistant Bacteria." Or, at least, they aren't the main driver of them. The only place you find those "Superbugs" is in hospitals, usually in people with seriously compromised immune systems. Ever since reading E.D. Weinberg's book, I have thought that iron status of the host was a major factor, seeing it was a discovery that iron could completely neutralize the effect of tetracycline that started his interest in iron research.

As such, I am dubious that these synthetic mRNA shots can develop a so called "Supervirus." I have repeated time and again that I haven't seen any proof of the discovery of a "novel corona virus" in December of 2019, and even if there was, that doesn't mean the virus was new, and it doesn't mean it made even a single person sick.

As such, while I think there is very good reason to avoid this round of mRNA beta testing on the population as a whole, and compromising the health of those who opt into the experiment, I don't think there's any evidence of a "Supervirus."
 

Bluemachine

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As such, while I think there is very good reason to avoid this round of mRNA beta testing on the population as a whole, and compromising the health of those who opt into the experiment, I don't think there's any evidence of a "Supervirus."
What are your concerns with the mRNA?
 

tankasnowgod

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What are your concerns with the mRNA?
You mean other than the fact that's only been tested for 28 days before being rolled out to the public when other drugs and vaccines are tested for four years?
Or the fact that it can't even rely on this history of other vaccines (dubious as they are), as this is completely new injectable tech?
Or the fact that it's put out by the same companies that sell drugs like SSRIs, Statins, and Vioxx?
Or the fact that it's for a virus that is basically the common cold?
Or the fact that any company or doctor that injects you with it has zero liability for any side effects, up to and including death?

Other than those..... none, really.
 

haidut

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You mean other than the fact that's only been tested for 28 days before being rolled out to the public when other drugs and vaccines are tested for four years?
Or the fact that it can't even rely on this history of other vaccines (dubious as they are), as this is completely new injectable tech?
Or the fact that it's put out by the same companies that sell drugs like SSRIs, Statins, and Vioxx?
Or the fact that it's for a virus that is basically the common cold?
Or the fact that any company or doctor that injects you with it has zero liability for any side effects, up to and including death?

Other than those..... none, really.

...Or the fact that the mRNA from the vaccine has been shown to be incorporated into human DNA, creating a GMO (us), and turning the newly created mutant into a machine for producing highly inflammatory spike proteins that generate all inflammatory requirements of CVD...except that it happens in a matter of weeks/months, instead of decades as with regular CVD onset.
 

gaze

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...Or the fact that the mRNA from the vaccine has been shown to be incorporated into human DNA, creating a GMO (us), and turning the newly created mutant into a machine for producing highly inflammatory spike proteins that generate all inflammatory requirements of CVD...except that it happens in a matter of weeks/months, instead of decades as with regular CVD onset.
but that study is of the virus itself, and don't all viruses come with the enzymes for reverse transcription? isn't that how they multiply? how do we know if the isolated mrna in a vaccine is able to do the same thing as the entire virus itself
 

StephanF

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The comment on the bioRxiv website by Albert Heim made most sense to me:



As a clinical virologist I am suprised about the introduction and background of the study which resulted in a (form my view) peculiar hypothesis (genomic integration of SARS-CoV-2). I don't want to comment on the way this hypothesis was tested, merely on its background.
Long term detection (several weeks to a few months) of any respiratory virus (e.g. Rhinovirus, Influenzavirus) after an acute infection is "business as usual". However, systematic follow up testing of these patients was not usual, but if a patient was diagnosed with Flu A in January and comes down with another respiratory infection in March, it is not surprising to detect e.g. HMPV and Flu A in March. If the analysis is done with real time PCR, you will find e.g. Ct 18 for HMPV and CT 37 for Flu A, so the diagnosis in March is "HMPV infection" and the detected Flu A is a little bit "left overs" from January.
In general: If you use multiplex PCR diagnostics about 5 to 10% of all diagnostic respiratory samples can be positive for two or three viruses, usually one of these is highly positive (the real culprit) and the other(s) are found close to the LOD (left overs of previous infections).
In COVID-19 patients, we follow up virus loads in respiratory specimens. These decline rapidly with convalescence but remain at levels close to the LOD (and therefore intermittently positive) for many weeks. This is an anticipated result as with other respiratory viruses. The respiratory tract contains hairs, mucus, tonsillary clefts, sinus and many other structures where a little bit of any "dirt" (e.g. a few of the billions of capsids produced in an infection) can persist. Even on "clean" surfaces (e.g. stainless steel) of a laboratory, you can find these viral contaminations by highly sensitive PCR if not meticulous decontamination measures were performed. No one would however build a hypothesis from this finding that SARS-CoV-2 has a specific mechansm to perist on (or: integrate in) stainless steel. Such a PCR result merely shows imperfect decontamination of a surface (but there are no decontamination at all done in the respiratory tract, neither brushing with SDS nor with sodium hypochloride nor flushing with fresh water as the least cleaning measure). Anyway, these results do not show infectious particles. Even if a few of these capsids were (theoretically) infectious, these were too few to cause an infection.”
 

Beatrix_

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Review J Virol 2023 Sep 1;e0065823. doi: 10.1128/jvi.00658-23. Online ahead of print.
Virus hijacking of host epigenetic machinery to impair immune response

CONCLUSION
Many studies have highlighted DNA methylation and histone PTM participation in the
modulation of viral infectivity, as well as host immune responses. While host defense
mechanisms have evolved and been enhanced over time through coexistence with
pathogens, viruses have also evolved to exploit host cellular immune behavior (85). By
modulating the host epigenome, viruses can improve their survival and subsequently
the associated pathogenesis.
Studies on coronaviruses highlight strong modulation of the host epigenetic
landscape to prevent immune responses, as described here (Table 1), but also to favor
infection through the modulation of key host proteins involved in the viral life cycle, as
described elsewhere (19, 86, 87). While not all members of the Coronaviridae modulate
the host’s epigenetic landscape in the same manner or to the same extent, other
mechanisms/targets are conserved between the genera, highlighting the signifi cance
of inhibiting the targeted pathway to establish and/or maintain their infection. However,
some of the epigenetic modulations mentioned in this review, although they counteract
the host immune response, are not suffi cient to prevent the elimination of the infection
(e.g., infl uenza A, adenoviruses). Nevertheless, epigenetic marks in the host cell can
be maintained for years and can contribute to changes characteristic of cancer develop
ment (34), highlighting the need to better understand the eff ect of the virus on the host
genome even after viral elimination. Therefore, reverting epigenetic changes made by
viruses should be considered as both a way to eliminate viral infection by re-enabling
the immune system to “fi ght back” and to prevent the development of associated
pathologies. Additionally, we hope to emphasize that the epigenetic modulation of host
immune responses by viruses has not yet been thoroughly studied from the perspective
of comparative evolution. As several viruses have co-evolved with their hosts, it is likely
that similar epigenetic modulation mechanisms or targets might have emerged over
time. Thus, we can hypothesize that some of the mechanisms described in this review
might also be discovered for other viruses in the future.
Moreover, in addition to epigenetics, viruses have evolved other ways to modulate
the quantity of host transcripts. Using miRNA or long non-coding RNA, either host or viral
encoded, viruses can subvert immune responses, as reviewed elsewhere (88, 89).
Epidrugs are drugs targeting epigenetic marks that are responsible for epigenetic
alterations, such as DNMTs altering DNA methylation, HDACs, HATs, or HMTs altering
histone acetylation or methylation levels (90). While most “epidrugs” aim to directly
rewire epigenetic modifi ers targeting the viral genome, it has been demonstrated that
some HDAC inhibitors (such as Trichostatin A) could upregulate IFNα-related pathways
during respiratory syncytial virus infection (91), thereby suppressing the infection. An
increasing number of epidrugs are being developed and tested worldwide, especially
for the treatment of cancer (90). While clinical trials for specific molecules take time,
preclinical studies on in vitro and in vivo models of infection should be considered. These
treatments could enable a potent immune response against viruses, allowing the host
to “fi ght back.” Furthermore, since these drugs aim to target the host genome and not
the viruses directly, drug resistance or manipulation of the host machinery to counteract
immunity are less likely to occur.
With an increasing body of evidence for epigenetic viral modulation of immune
pathways, epigenetic-targeted therapy off ers an appealing option to overcome latency
and replication, which could, in turn, lead to potential benefi ts vis-à-vis control of the
infection and associated pathological complications.


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