COVID-19 vaccine(s) makes people test positive on an HIV test

[b555]

I already responded to a similar critique by user "hei". First of all, we don't know if the patients responded to the HIV fragment of they started generating the full HIV particle endogenuosly. The vaccine does not contain enough "gp41" in itself to trigger a response only to it. If it had enough viral protein to trigger antibody production then most/all of the trial participants would have tested positive. Second of all, the "verification" that the patients were "fine" after they tested positive violates the standard protocol for confirming HIV infection after a first positive test. The standard way to confirm/reject HIV diagnosis is to follow these patients for 3-6 months then retest at least once a few months after the initial positive test. If that test is also positive then the official rules say these people have chronic HIV infection. Those tests were not done, and in fact, the only information I can find on what "routine tests" for HIV were done suggest only PCR tests were done. Those have a 20%+ false negative rate and, again, are NOT the standard way to confirm/reject HIV infection.
One can't just pick and choose when antibody tests apply and when they do not. Either the standard HIV tests work and need to be used on those 4 patients according to the standard protocol for HIV testing, or those tests are useless, in which case the question is what exactly are they measuring in the millions of people to who they are administered. Why can't some of the millions of HIV positive people around the world have also come into contact with another exosome or virus that can trigger a positive HIV test without that actually being a true infection??? @tankasnowgod voiced similar concerns earlier in the thread.
Furthermore, when the vaccine authors say themselves that "significant changes would need to be made to well-established HIV testing procedures in the healthcare setting to accommodate rollout of this vaccine", that speaks volumes by itself about its safety. Speaking of safety, why was the trial immediately halted and vaccine development abandoned if this is all just a harmless "false positive"??
Finally, I specifically asked Peat during out latest podcast if the COVID-19 vaccines can trigger an AIDS-like condition and he said emphatically "YES". His quotes on the dangers of activating the retroviruses in our genome is in the original post.
All in all, until the standard protocols for confirming/rejecting chronic HIV infection are followed, the HIV test results stand and these people are by law considered HIV positive. Either that, or the whole HIV testing mechanism is a charade.

@haidut The vaccine contained no genetic material because it was a protein vaccine. Therefore it cannot produce an infection of any kind because protein cannot replicate without genetic material (DNA/RNA) with the exception of prions, which is not applicable here. Every patient will produce antibodies to different epitopes (segments) of the vaccine protein. If they produce an antibody to an epitope that is in common with HIV then they will likely test positive for HIV in the future. This would indeed make the HIV antibody test useless. That said, not everyone will generate antibodies to those epitopes so not everyone will test positive.

We can use a generic antibody test to detect HIV infection because there is no vaccine for HIV. If there were a vaccine for HIV, like there is for Hepatitis B, then a surface antibody test would indicate immunity either through vaccination or infection. That’s why we have a core-specific antibody test for hepatitis B to differentiate vaccination status from history of infection. We would have to create a similar test for HIV if we’re going to start vaccinating people with fragments of HIV’s coat. It is easier to simply abandon this vaccine given other promising candidates.

 

[LeeLemonoil]

@b555

What is the rationale behind having such epitopes on the proteins used in the experimental vaccine?
Is there an inherent necessity to it, like the only proteins that elicit adequate immune response for immunization have by default these epitopes and cant be altered?

Or is it by design, and then: couldn’t that be avoided?

As you say, it’s at the very least idiotic to render HIV-antibody tests virtually useless in the future because of mass-vaccination for another illness when there are alternatives

 

[b555]

@LeeLemonoil Great question. It’s very cutting edge so I don’t know all the details, but from what I can glean from a paper on it I’ll link to below, producing the COVID protein vaccine in cells through traditional means can limit yield and immunogenicity because its shape gets altered when being exported through the cell membrane. The HIV gp41 peptides act as a “molecular clamp” that keeps the vaccine conformation stable through the intercellular production process so that the collected vaccine is more similar in shape to the spike protein of actual COVID. In another questionable metaphor, if Brad Pitt is COVID and I’m the Australian protein vaccine, if you’re exposed to me as I am and later see Brad Pitt, you probably wouldn’t think Brad Pitt is me. However, if I borrow a special belt from HIV to suck in my belly to look more like Brad Pitt, you’d be more likely to confuse Brad Pitt for me later and try to attack him, as I assume you would want to attack me. The vaccine creators were hoping your immune system wouldn’t notice the belt as it is quite small, but some people’s immune systems did and now recognize the belt when they’re tested for HIV. Rapid Response Subunit Vaccine Design in the Absence of Structural Information

 

[pro marker]

ive havent looked much into this, anyone here care to share their opinions on aajonous theory that aids was created in a lab in america, and then laced onto needles, causing the huge ammount of aids in gay people? according to his "research" the only way to get aids is to inject it.

 

[LeeLemonoil]

@LeeLemonoil Great question. It’s very cutting edge so I don’t know all the details, but from what I can glean from a paper on it I’ll link to below, producing the COVID protein vaccine in cells through traditional means can limit yield and immunogenicity because its shape gets altered when being exported through the cell membrane. The HIV gp41 peptides act as a “molecular clamp” that keeps the vaccine conformation stable through the intercellular production process so that the collected vaccine is more similar in shape to the spike protein of actual COVID. In another questionable metaphor, if Brad Pitt is COVID and I’m the Australian protein vaccine, if you’re exposed to me as I am and later see Brad Pitt, you probably wouldn’t think Brad Pitt is me. However, if I borrow a special belt from HIV to suck in my belly to look more like Brad Pitt, you’d be more likely to confuse Brad Pitt for me later and try to attack him, as I assume you would want to attack me. The vaccine creators were hoping your immune system wouldn’t notice the belt as it is quite small, but some people’s immune systems did and now recognize the belt when they’re tested for HIV. Rapid Response Subunit Vaccine Design in the Absence of Structural Information

Thanks.. I really hope the designers and researchers do this bcuase to their best knowledge and abikity this is their means to achieve sufficient immunogenicity.

Which leaves the question: How limited is (their) or general knowledge in such virus-related biotech matters that the filed isn't able to come up with another protein clamp. VEry limited is my guess. They likely know this stuff and use it becuase HIV is well researched and ha to default back on canonical knowledge. I would opt out of such a vaccine.

THe modiefied mRNA stuff on the other hand also has mayn question marks behind it.

Need look up what other vaccines are likely to reach the market for covid with other techs. I dont know if the vector based vax have modRNA in tem or "nromal" mRNA

 

[haidut]

@haidut The vaccine contained no genetic material because it was a protein vaccine. Therefore it cannot produce an infection of any kind because protein cannot replicate without genetic material (DNA/RNA) with the exception of prions, which is not applicable here. Every patient will produce antibodies to different epitopes (segments) of the vaccine protein. If they produce an antibody to an epitope that is in common with HIV then they will likely test positive for HIV in the future. This would indeed make the HIV antibody test useless. That said, not everyone will generate antibodies to those epitopes so not everyone will test positive.

We can use a generic antibody test to detect HIV infection because there is no vaccine for HIV. If there were a vaccine for HIV, like there is for Hepatitis B, then a surface antibody test would indicate immunity either through vaccination or infection. That’s why we have a core-specific antibody test for hepatitis B to differentiate vaccination status from history of infection. We would have to create a similar test for HIV if we’re going to start vaccinating people with fragments of HIV’s coat. It is easier to simply abandon this vaccine given other promising candidates.

Even if all of this is true, generation of antibodies to an HIV fragment is hardly a desirable effect. Also, I am far from convinced that introduction of HIV fragments through a vaccine is even remotely safe. See the study below demonstrating that "gp41" has a very important role in facilitating an HIV infection.
Do you really think the vaccine development was stopped due to "practical" reasons such as existence of more effective alternatives? In my experience, drug development does not get abruptly dropped after millions in sunken costs unless there is a very good reason, and until I see more evidence to the contrary (and especially considering the link below) my money is that the vaccine was dropped due to safety concerns associated with HIV.

@LeeLemonoil @Drareg @hei @tankasnowgod @boris

HIV-1 Envelope gp41 Peptides Promote Migration of Human FcεRI+ Cells and Inhibit IL-13 Synthesis Through Interaction with Formyl Peptide Receptors

We evaluated the effects of synthetic peptides (2017, 2019, 2020, 2021, 2023, 2027, 2029, 2030, 2031, and 2035) encompassing the structure of HIV-1MN envelope gp41 on both chemotaxis of human basophils and the release of preformed mediators (histamine) and of cytokines (IL-13). Peptides 2019 and...

www.jimmunol.org

"...This study demonstrates that two ectodomain peptides of HIV-1 envelope gp41MN, 2019 and 2021, are potent chemoattractants for human FcεRI+ cells. Moreover, these two peptides selectively inhibit the release of preformed mediators and of cytokines from human basophils activated by FMLP. This is the first demonstration that ectodomain peptides of HIV-1 gp41 are functionally active on human FcεRI+ cells presumably through interaction with FMLP receptor(s). Increasing evidence indicates that human FcεRI+ cells could be involved in HIV-1 infection in a variety of ways (11, 12, 13, 14, 15, 16). In fact, we have demonstrated that gp120 from divergent HIV-1 isolates from different clades interacts with the VH3 region of IgE on human FcεRI+ (9, 47). The superantigenic interaction between gp120 and IgE leads to the synthesis and release of IL-4 and IL-13 from FcεRI+ cells (9). In addition, we found that the HIV-1 Tat protein is a potent chemoattractant for human FcεRI+ cells and up-regulates the expression of CCR3 on these cells (10). These results demonstrate that two distinct HIV-1 proteins, gp120 and Tat, can activate human FcεRI+ cells through different immunologic mechanisms.
Human basophils, but not mast cells, also express receptors for FMLP which induce their chemotaxis and the release of proinflammatory mediators (35, 38, 40). Three FPRs have been identified on different cells (28, 29). These receptor subtypes belong to the STM, G-protein-coupled Rhodopsin superfamily (50, 51). The FPR has a high affinity for FMLP and is activated by picomolar concentrations of FMLP. FPRL1 is a promiscuous receptor activated in response to higher concentrations of FMLP (50), lipoxin A4 (33), H. pylori peptide Hp (2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20) (34), serum amyloid A (32), and by different synthetic peptides (29). Human monocytes express FPRL2 and Hp (2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20) is chemotactic through the activation of this receptor subtype (29). The distribution of FPR subtypes in human basophils and their biological significance in immune responses in HIV-1 infection remain to be established.
The results of our experiments reveal that interactions between gp41 peptides and FMLP receptors expressed on human basophils are more complex than hitherto believed. CsH is known to block FPR-evoked responses (29, 35, 36). Accordingly, CsH blocked the chemotactic activity of FMLP on basophils, but had no effect on the response evoked by gp41 peptides 2019 and 2021. To try to clarify the specificity in the activation route for gp41 peptides and FMLP, we performed cross-desensitization experiments. Upon binding of FMLP to its FPR, the occupied receptor is phosphorylated (52). Cells are subsequently desensitized and unable to generate signals through the same receptor. We have demonstrated that basophils preincubated with FMLP in the absence of Ca2+ were unable to generate a chemotactic response when rechallenged with the same agonist in a Ca2+ containing buffer (homologous desensitization). Similarly, basophils preincubated with gp41 peptide 2019 or 2021 were desensitized to a subsequent challenge with the homologous stimulus. Heterologous desensitization provides interesting and apparently contrasting results. When basophils were preincubated with a low concentration (5 × 10−7 M) of FMLP, which binds with high affinity only to FPR, but not to FPRL1 (50), the chemotactic response to heterologous stimulus (gp41 2019) was not affected. In contrast, when basophils were exposed to high concentrations (10−4 M) of FMLP, which binds also to FPRL1 (50), the chemotactic response to gp41 2019 was significantly reduced. The results of these two groups of experiments are consistent with the hypothesis that gp41 peptides and FMLP act through different FPR subtypes to induce chemotaxis of human basophils: FMLP acts essentially through the interaction with FPR, whereas gp41 peptides presumably act through FPRL1. This hypothesis is supported by the different pharmacologic effect of CsH on basophil chemotaxis induced by FMLP and gp41 peptides. Interestingly in this context, recent experiments performed in our laboratory have demonstrated the presence of FPRL1 mRNA in human basophils (data not shown).
Several investigators have started to examine the complexity of interactions of HIV-1 gp41 peptides and FPRs expressed on human phagocytes. It was found that the retroviral-derived exapeptide LDLLFL is a potent inhibitor of FMLP-induced responses of human monocytes and granulocytes (53). Lawless et al. (54) reported that two synthetic peptides, designated T21 and T20, corresponding to amino acid sequences 558–595 and 643–678, respectively, in HIV-1LAI gp41, are strong inhibitors of HIV-1 viral fusion. Ueda et al. (25) reported that HIV-1 envelope gp41 is a potent inhibitor of chemotaxis induced by FMLP in human monocytes. The same group of investigators reported that T21 activates human phagocytes by using FPR and FPRL1 (26). It was also found that synthetic T20 analogs lacking N-terminal amino acids acted as FPR antagonists (27). Furthermore, a synthetic peptide corresponding to amino acid residues 414–434 down-regulates the expression of CCR5 and CXCR4 receptors by activating FPRL1 (55). Finally, a synthetic exapeptide (Trp-Lys-Tyr-Val-d-Met) that uses both FPR and FPRL1 acts as a potent agonist to stimulate human phagocytes (50, 51) with preference for FPRL1 (51). Taken together, these findings emphasize the different effects of retroviral-derived peptides on human immune cells. In addition, they indicate that natural and synthetic peptides can act as either agonist or antagonist at the FPR level.
Our findings demonstrate also that prolonged incubation with low concentrations of peptides 2019 and 2021 of HIV-1 envelope gp41 of the mn strains inhibits the release of preformed mediators and of cytokine synthesis from human basophils activated by FMLP. Although several synthetic peptides encompassing the structure of HIV-1MN envelope gp41 do not activate the release of cytokines and proinflammatory mediators from human basophils, peptides 2019 and 2021 specifically antagonize the activation of basophils induced by FMLP. These novel results are of interest for several reasons. First, they show that gp41 peptides 2019 and 2021 exert different effects on basophil chemotaxis and on mediator secretion from these cells. In fact, in the former system the peptides induce basophil chemotaxis presumably by interacting with FPRL1. In the latter system, low concentrations of peptides 2019 and 2021 are devoid of any activating property on the release of mediators, but they antagonize the releasing activity of FMLP on basophils. Interestingly, the inhibitory effect of peptides 2019 and 2021 on FMLP-induced basophil activation is not immediate and requires a long preincubation time (35–60 min). This lag could be necessary to activate/deactivate certain metabolic steps or to cause FMLP receptor internalization.
Taken together, these results might suggest that the chemotactic activity and the release of mediators from basophils induced by FMLP and gp41 peptides are mediated by activation of different FPR subtypes. Alternatively, the possibility exists that signal transduction mechanisms underlying chemotaxis and secretion are differently activated, inhibited and/or modulated by gp41 peptides and FMLP. Finally, it might be that FMLP and gp41 peptides, in addition to FPR, FPRL1 and FPRL2, activate or antagonize additional unknown receptor(s) on basophils. Whatever the mechanisms, our findings leave no doubt as to the complexity of the interactions between FMLP, gp41 peptides, and FMP subtypes in human basophils.
During HIV-1 infection, the envelope gp160 is enzymatically cleaved, yielding two mature proteins, the transmembrane gp41 and surface gp120 (56, 57). HIV-1 infection is initiated by high-affinity binding of gp120 to CD4, the primary receptor for HIV-1 (58, 59). gp41 is thought to mediate fusion between viral and cellular membranes by the insertion of hydrophobic N terminus into the plasma membranes (57, 60). Several lines of inquiry indicate that gp41 also may exert multiple effects on the host immune system. Soluble gp41 has been shown to induce the release of proinflammatory cytokines (TNF-α and IL-1) (17, 18, 19, 20, 21), to suppress lymphocyte proliferation (23) and to induce IL-10 in monocytes (24). gp41 has been detected in brain tissues of patients affected by AIDS dementia (22) and Abs recognizing various epitopes of gp41 appear at early stages of HIV infection (61). Moreover, it has been reported that monocytes and neutrophils from HIV-1-infected patients responded poorly to a variety of chemoattractants, including FMLP (62, 63, 64, 65, 66). The interaction of gp41 peptides with FPRs on human basophils might be of clinical relevance in patients with HIV-1 infection.
We previously demonstrated that gp120 directly induces the release of preformed mediators and of cytokines (IL-4 and IL-13) from human basophils purified from healthy individuals (9). In this study, we found that another envelope glycoprotein, gp41, can interfere with cytokine production by inhibiting the synthesis of cytokines induced by FMLP in human basophils. Together these findings indicate the complexity of the interaction between HIV-1 envelope peptides and human FcεRI+ cells. The biological significance in host defense and immune responses in HIV-1 infection of our findings requires additional investigations.
In conclusion, we provide the first evidence that two envelope gp41 peptides are potent chemoattractants for human FcεRI+ cells and inhibit FMLP-induced mediator release from human basophils. Because HIV-1 enters the body predominantly through mucosal surfaces and because early phases of infection are associated with high levels of viremia, basophils can be exposed to high local levels of envelope gp41 peptides. This suggests that FcεRI+ cells can contribute, also through this novel mechanism, to the dysregulation of the immune system in HIV-1 infection."

 

[LeeLemonoil]

At least they dropped it (for now?)

It goes to show that with every new vaccine campaign looming in the future we need to do diligent research what they put into it.

I’m dreading the days when „painless“ Nano-Injektion are ready. So many wonderful potential uses.

So much potential for endless harm

 

[Gone Peating]

ive havent looked much into this, anyone here care to share their opinions on aajonous theory that aids was created in a lab in america, and then laced onto needles, causing the huge ammount of aids in gay people? according to his "research" the only way to get aids is to inject it.

How would the virus survive for that long? I’m not denying it’s possible I just thought viruses can’t survive for very long outside the body

 

[Gone Peating]

Aside from being unreliable and uncomfortable is there any danger in the covid swab tests?

 

[LeeLemonoil]

Aside from being unreliable and uncomfortable is there any danger in the covid swab tests?

No. If you wanna be completely certain make sure you see the staff opening fresh swap package to avoid any sort of contamination

 

[pro marker]

Aside from being unreliable and uncomfortable is there any danger in the covid swab tests?

No. If you wanna be completely certain make sure you see the staff opening fresh swap package to avoid any sort of contamination

i am almost certain they are spreading covid through the swab tests. absolutely do not get tested unless you have to is what i say. there was also a news article about swabs accidentally being infected.

 

[b555]

@haidut @LeeLemonoil
Protein folding is very complicated and time consuming to research. Repurposing motifs that have been well studied with known effects is common. For example, a fragment of human antibodies called Fc is often attached to therapeutic proteins to prolong the amount of time they can last in circulation without be degraded. Developing de novo, functional protein fragments like that would take years. It would be akin to reinventing the natural-occurring wheel.


As I said, generating antibodies to the HIV fragment was not a desirable effect. It does not cause adverse health effects but it would invalidate current HIV testing protocols. Therefore, this vaccine was abandoned. Again not a safety concern, but detrimental in the sense that it would make detecting HIV infections more difficult.

 

[Gone Peating]

i am almost certain they are spreading covid through the swab tests. absolutely do not get tested unless you have to is what i say. there was also a news article about swabs accidentally being infected.

Could the virus survive? I always thought viruses die very quickly outside a host

 

[LeeLemonoil]

@haidut @LeeLemonoil
Protein folding is very complicated and time consuming to research. Repurposing motifs that have been well studied with known effects is common. For example, a fragment of human antibodies called Fc is often attached to therapeutic proteins to prolong the amount of time they can last in circulation without be degraded. Developing de novo, functional protein fragments like that would take years. It would be akin to reinventing the natural-occurring wheel.


As I said, generating antibodies to the HIV fragment was not a desirable effect. It does not cause adverse health effects but it would invalidate current HIV testing protocols. Therefore, this vaccine was abandoned. Again not a safety concern, but detrimental in the sense that it would make detecting HIV infections more difficult.

Thanks, I thought as much

 

[LeeLemonoil]

i am almost certain they are spreading covid through the swab tests. absolutely do not get tested unless you have to is what i say. there was also a news article about swabs accidentally being infected.

Millions upon millions were swab tested, much more then there are confirmed cases. Nobody is doing such a thing deliberately.

 

[Gone Peating]

Millions upon millions were swab tested, much more then there are confirmed cases. Nobody is doing such a thing deliberately.

There’s speculation that they put the vaccine or some type of tracking nanotech in the swabs. What are people’s thoughts on the possibility of this?

 

[Gone Peating]

@charlie for some reason this thread isn’t showing up on the main page even though there are very recent comments

 

[charlie]

@charlie for some reason this thread isn’t showing up on the main page even though there are very recent comments

You need to adjust your filters. Basically "uncheck" everything.

 

[Soren]

@haidut @LeeLemonoil
Protein folding is very complicated and time consuming to research. Repurposing motifs that have been well studied with known effects is common. For example, a fragment of human antibodies called Fc is often attached to therapeutic proteins to prolong the amount of time they can last in circulation without be degraded. Developing de novo, functional protein fragments like that would take years. It would be akin to reinventing the natural-occurring wheel.


As I said, generating antibodies to the HIV fragment was not a desirable effect. It does not cause adverse health effects but it would invalidate current HIV testing protocols. Therefore, this vaccine was abandoned. Again not a safety concern, but detrimental in the sense that it would make detecting HIV infections more difficult.

Calls into question HIV testing in general. I've read many horror stories of false positives for HIV. Still I am staying a million miles away from this vaccine and I have advised everyone I know to do the same. God only knows what is in it these pharmaceutical companies are despicable.

I'm curious perhaps you have already answered this elsewhere. Do you plan on taking the vaccine and do you think people should take it?

 

[boris]

Millions upon millions were swab tested, much more then there are confirmed cases. Nobody is doing such a thing deliberately.

CDC’s failed coronavirus tests were tainted with coronavirus, feds confirm​

The same thing happened in England. Now those are only the occurences where it came out because it got investigated. Impossible to say for us where else it happened or if it is still happening.

The CDC knew that those tests were bunk and released them anyways.