Diabetes Drug makes "HIV" PCR test Negative

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Thank you to subscriber Jeff R for posting me this interesting piece it certainly seems to backup my hypothesis or rather the scientific establishments own data that says that PCR tests are not measuring specific nucleotide sequences but are instead measuring charge:

How many people are HIV positive?

Globally, the most recent data shows:

• About 40.8 million people worldwide are living with HIV (as of 2024)

A bit more context

• Around 1.4 million of those are children (under 15)

• Roughly 39 million are adults

• About 0.7% of adults globally are HIV-positive

Important to understand

• HIV is still a major global health issue, but treatment has improved a lot

• Many people with HIV live long, healthy lives thanks to antiretroviral therapy (ART)

• Around 77% of people with HIV are receiving treatment.

When “In the field” and people are being monitored for their “HIV” treatment, every so often you will find naughty people such as Kevin Brau, friend to the Virology Control Studies Project who wakes up to the scam of Virology and stops taking their harmful Anti Retro Viral Medication that the medical establishment are claiming are keeping them alive. In this and many many other incidence, failure to then register an “HIV” PCR positive (Which should be 100% without ARVs as they claim “HIV” has integrated into their “Genome”) leaves them with severe egg on face.

As the data shows, they claim an absolutely gobsmacking level to the “HIV” fraud that there are some 40million people scammed into believing they have some permanent “Infection” that will kill them unless they hand over money to Gilead. An interesting addendum to this is that HIV.Gov the home for official “HIV” statistics, lists the current number of people that have a claimed “HIV” positive status but are not taking Anti Retro Viral medication is 10 Million. Well, that is a highly encouraging number of control experiments, living, breathing and walking around being a thorn in the side of the medical establishments scare stories for everyday they live on.

These living, breathing data anomalies are a particular problem for the Medical Establishment and Big Pharma (Same thing alert). They claim that “HIV” has permanently integrated into their genome so they should either take their drugs or face a swift death (Fantastic business model if you can find it, right… “Pay us or die”). When there are people that are not listening to these Mafioso tactics and continue to live a healthy (likely more healthy than before) life, they need to find excuses for why this is happening.

The first, which we have covered in a good amount of detail on the Virology Control Studies Project is what they hilariously dub “Elite Controllers”, people whom have magic “DNA” that can do jiggery pokery to the “HIV” to make the test negative without drugs. Interestingly this Magic “DNA” didn’t work in the first place when they got onboarded to the Allopathic Death Cult because they must have tested positive up front to be tracked as an “HIV Infected” individual. A slight variation on this systemic control failure of the PCR, is what they call “Long Term Non Progressors”. They don’t have the Magic “DNA” to make the tests Negative, no their tests are still positive, but what they do have is a slightly different Magic “DNA” that means that the high “Viral Load” of the tests mysteriously do nothing to their health, so they live perfectly healthy whilst the tests are pinging off the charts telling them they are going to be dying any second now.

So we know that they are always on the lookout for fantastical stories to explain away their abject failure in the field. What we are going to be looking at today, very briefly is a new news story that represents yet another one of those scapegoats for failure in the form of a Diabetes Drug, Metformin:

Scientists are investigating why a small number of people with HIV can keep the virus suppressed long after stopping treatment, uncovering clues within the immune system. Their findings point to specific immune cells and genes that help maintain this dormant state.

Researchers found that certain immune cells, genes, and the drug metformin may help keep HIV dormant after treatment stops, offering new paths toward long-term control.

For millions of people living with HIV, taking daily medication is essential for life. If treatment stops, the virus typically returns within weeks.

However, some rare individuals can control the virus for months or even years after stopping therapy, a phenomenon that has puzzled scientists.

“Strikingly, a small number of people rebound much more slowly and take multiple months or even longer to rebound,” says Nadia Roan, PhD, senior investigator at Gladstone Institutes.

A team of Gladstone scientists—including Ashley George (left) and Nadia Roan (right)—uncovered a new path toward life without daily HIV pills, suggesting that a common diabetes pill could help achieve long-term remission. Credit: Gladstone Institutes

New Clues to Long-Term HIV Control

In research published in Immunity, Roan and her colleagues offer new insights into this effect and highlight possible ways to maintain long-term health without ongoing antiretroviral therapy.

One key discovery is that two genes inside infected cells act like protective locks that keep HIV inactive. The team also found that metformin, a widely used diabetes drug, can activate one of these mechanisms to help maintain the virus in a dormant state.

George and her colleagues found that treating HIV cells with metformin blocked the virus’s ability to reactivate, suggesting a possible role for this drug in delaying, or even preventing, HIV. Credit: Gladstone Institutes

“Our data suggest metformin might be able to delay, or possibly even prevent HIV rebound in some individuals, which is exciting because it’s a very safe and affordable drug,” says Roan, senior author on the study. “We are now very interested in pushing forward with preclinical and eventually clinical studies to directly test these potential benefits.”

Hidden HIV Reservoirs and Rebound Risk

Although antiretroviral therapy can suppress HIV, it does not eliminate it. The virus remains hidden in “reservoir” immune cells that contain its genetic material. If treatment is interrupted, these reservoirs can produce active virus again, leading to renewed symptoms and potentially acquired immunodeficiency syndrome (AIDS).

To better understand how some individuals keep the virus under control, the researchers examined people who maintained suppression after stopping treatment.

They analyzed four clinical trials in which participants paused therapy under close medical supervision, often as part of efforts to test potential HIV cures.

Immune Cell Analysis Reveals Key Patterns

The team studied blood samples from 75 participants collected just before treatment stopped, measuring gene and protein activity across different immune cell types to identify patterns linked to delayed viral rebound.

Their analysis revealed several important findings. In two trials, individuals with higher levels of stem cell memory CD8+ T cells experienced slower viral return. The two participants with the longest delays, more than 22 weeks and over 33 weeks, had the highest levels of these cells.

The study by George (left) and Roan (right) is part of a broader effort by a multidisciplinary group of researchers, named the HOPE Collaboratory, working to cure HIV. Credit: Gladstone Institutes

“These CD8+ T cells appear to have ‘stem-like’ features and might be able to stick around to continue replenishing themselves for prolonged periods of time, which may help them contribute to long periods of ART-free HIV control,” Roan says.

Role of Natural Killer Cells in HIV Control

In another trial, people with an unusual form of natural killer cells also showed delayed rebound compared to those with the typical type. While these cells are known for destroying infected cells, they can also influence how other immune cells function, which may affect how quickly HIV returns.

“Altogether, our findings suggest there’s probably not just one solution for suppressing HIV,” says Ashley George, PhD, research scientist at Gladstone and co-first author on the study. “By leveraging different features of immune cells that can help fight infection, we likely have multiple opportunities to control HIV without the need for ART.”

The researchers also identified important changes in CD4+ T cells, the main type of cell that serves as an HIV reservoir.

Genes That Help Keep HIV Dormant

Higher levels of two genes, DDIT4 and ZNF254, were linked to longer delays before the virus rebounded. Laboratory experiments confirmed that both genes can suppress HIV activity.

“Both genes represent possible new targets for a promising ‘block and lock’ strategy for curing HIV, in which drugs would first be used to block HIV activation, followed by ways to make this block permanent,” George says.

This strategy is central to the work of the HIV Obstruction by Programmed Epigenetics (HOPE) Collaboratory, a research group focused on finding a cure.

By studying the rare individuals who continue to suppress the virus even after treatment ends, Roan (left) and her team identified features of immune cells that can keep the virus locked down. Credit: Gladstone Institutes

Further analysis of existing data supported these findings. Individuals with higher levels of the two genes showed reduced viral activity, and “elite controllers,” people who naturally suppress HIV without treatment, had especially high levels of ZNF254 in their CD4+ T cells.

“One possibility we’re imagining for the future is that we could somehow deliver ZNF254 to infected cells in order to turn people into elite controllers,” George says. “We could also try to engineer an even stronger version of this gene.”

Among all the findings, the link between DDIT4 and delayed viral return may have the most immediate clinical relevance. Levels of this gene can be increased by metformin, something previously observed in other cell types and now confirmed in T cells by this study.

Metformin’s Potential to Suppress HIV

This led researchers to test whether metformin could directly suppress HIV. In one experiment, the drug prevented the virus from reactivating in cells taken from people with HIV, suggesting it could support the “block and lock” approach.

The team plans to continue testing metformin and similar compounds in pre-clinical models to see if they can stop HIV from re-emerging when treatment is paused.

Drugs that keep HIV inactive could also benefit people who remain on therapy by reducing exposure to viral gene products that contribute to chronic inflammation.

“We are excited to pursue HIV silencing strategies both as a way to achieve block and lock, but also as a strategy to improve the overall health of people with HIV by lessening chronic inflammation,” Roan says.

Summary

Immunological mechanisms regulating HIV rebound after antiretroviral therapy (ART) interruption remain unclear. We examined relationships between host factors, HIV reservoir, and HIV time-to-rebound after analytical treatment interruption (ATI) by characterizing pre-ATI peripheral blood mononuclear cells (PBMCs) from 75 ART-suppressed people with HIV (PWH) using high-parameter methods. Across interventional (CLEAR, TEACH, and REDUC) and non-interventional (A5345) cohorts, delayed rebound was not associated with intact HIV. Cohort-specific immune effectors were associated with delayed rebound. RNA sequencing of CD4⁺ T cells from A5345 revealed that the mTOR inhibitor DDIT4 and zinc finger protein ZNF254 were associated with delayed rebound. In vitro and in vivo studies demonstrated that DDIT4 and ZNF254 suppressed HIV expression. Metformin induced DDIT4 and suppressed HIV expression in primary cells and cells from ART-suppressed PWH, suggesting that this affordable diabetes drug could be repurposed to silence HIV. Our results support the pursuit of both immune- and HIV-silencing strategies to achieve ART-free HIV remission.

ANALYSIS

First off the surprising thing is that they managed to find a fairly sizable cohort of “HIV” Positive individuals who were willing to stop their ARV meds. In the name of Soyence and all that I am sure they just put their trust in the priests in white coats, but still it is moving in the right direction that they are not piss scared of doing it.

For this study that is linked in the paper above they took 75 people and stopped ARVs and studied how long it took for them to “Rebound” from undetectable “Viral” load. On the face of it, even this part of the study was very useful as they set the bar for “Rebound” low at 1000 copies and despite this, some of the participants went for nearly 8 months before breaching this threshold. You must factor in that the people on this trial were likely the must gutter form of Pharmaceutical superfans being on this trial and being “HIV” Positive, so it is not likely they are going to be interested at all in naturally detoxing and bringing themselves back to balance (Which is what Elite Controlling is).

Now this trial has gone the typical convoluted route stopping off at their tried and tested course of bafflement in the form of “Genetics” where they make up random numbers and codes based on lab values and claim this has any mark on reality. Oh of course, silly me, the DDIT4 and ZNF254 are expressing like a runaway train in the Long term non progressors. Sigh. They then have the Eureka moment that one of them realized that a completely different drug for a completely different disease has something to do with this random lab value so they must “work” on both. I mean for once I think this is actually Logical “chemistry” where we are usually being told that, when it comes to killing stuff, like Ivermectin the same chemistry somehow weaves around the human that swallowed it and just goes to the little worm it was “programmed” to get.

WHAT IS METFORMIN?

Metformin’s origin traces back to a plant called Galega officinalis (also known as French lilac or goat’s rue), which was traditionally used to treat symptoms of diabetes.

Scientists later identified compounds in this plant (called guanidines) that lower blood sugar, which eventually led to the development of metformin.

Metformin is very much tied to charge and ionic behavior, and that’s actually central to how it moves around the body.

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Is metformin a charged molecule?

Metformin (Metformin) is a strongly basic compound, meaning it readily picks up protons (H⁺).

• At normal physiological pH (~7.4), metformin is positively charged

• In fact, it usually exists as a dication (carrying +2 charge)

Chemically, this comes from its guanidine groups, which are highly proton-attracting.

👉 In medicines, it’s almost always given as metformin hydrochloride, which is an ionic salt.

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What that means in practice

1. It doesn’t cross membranes easily

Because it’s charged and very water-soluble, metformin:

• Cannot diffuse freely through cell membranes (which prefer neutral, lipid-soluble molecules)

• Instead relies on transport proteins

Key ones include:

• OCT1 (organic cation transporter 1) in the liver

• OCT2 in the kidneys

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2. It accumulates in certain tissues

Those transporters actively pull metformin into cells, especially:

• Liver (main site of action)

• Kidneys (for elimination)

This selective uptake is why it mainly affects liver glucose production.

1. Metformin’s charge: why it matters so much

Metformin (Metformin) is a strong organic base. At physiological pH (~7.4):

• It is fully protonated

• Exists mainly as a dication (2+)

Structural consequence

Because it is:

• Highly charged

• Very polar

• Hydrophilic

👉 It cannot passively diffuse across lipid membranes

This is unusual for a drug that must act inside cells.

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So how does it get in?

It depends on transport proteins, mainly:

• OCT1 (Organic Cation Transporter 1) → liver uptake

• OCT2 → kidney handling

• Additional MATE transporters for excretion

These are electrogenic or facilitated transporters that recognize positively charged molecules.

Key insight:

Metformin’s charge is not a limitation—it is the “ticket” that allows selective transport into specific tissues.

Key takeaway

• Metformin’s positive charge is essential, not incidental—it determines tissue targeting via transporters.

• Its effects are fundamentally about creating a controlled cellular energy stress signal.

CONCLUSION

So they have taken a drug that was meant to work for a completely different disease in a completely different way, they have added it to a cell culture of “HIV” infected cells and shown that the addition of this drug suppresses “Viral Load” i.e it makes PCR test negative. Below is the simplified workflow from the paper:

🧫 A. Infection of primary human CD4⁺ T cells (main model)

Step-by-step:

1. Isolate primary CD4⁺ T cells

   • From healthy donors (and sometimes HIV+ donor samples in other experiments)

2. Activate the cells

   • With CD3/CD28 stimulation (to mimic immune activation)

3. Infect with HIV-1

   • They used a replication-competent HIV strain (NL4-3/BaL variants)

   • This allows full viral life cycle in cells

4. Add metformin at different doses

   • Typically ~0.5–1 mM (physiological in vitro range)

5. Culture for several days (up to ~12 days)

6. Measure outcomes using multiple readouts:

   • Flow cytometry (HIV p24 protein in cells)

   • ELISA (viral particles in supernatant)

   • PCR (viral DNA integration / early replication intermediates)

Where this becomes very interesting is highlighting exactly how Metformin is claimed to work, or rather its exact physical properties. Because this is what I am really talking about when I am simplifying the fraud of “Bio”Chemistry. When you actually lay all of these proposed chemicals out they really only differ in their physical properties i.e the measurable attributes; their charge, viscosity, polarity, density, state, colour, odor and volatility. Only a few of those are active and so …. well define its actions rather than its “existence”. So when we have a drug that has absolutely nothing to do with the claimed effectiveness of its original design used for a different process we must conclude that it is due to its measurable, definable properties that are causing this crossover.

In this case the most apparent property is that of its charge, which is noted as its most defining characteristic of its function. It is measured as being highly Basic in its pH, highly charged, very polar and hydrophilic, all of these things actually being able to be reduced to just charge as dealing with H+ Ions with pH, Polarity which is charge “distribution” and Hydrophilicity being a combination of polarity and charge.

So let’s marry this up with the theoretical work put out on the Virology Control Studies project. It is not really debatable that ultimately PCR is testing for Charge as it is verified in Gel Electrophoresis as outlined in the article “What is the PCR really testing for?” . It is specifically testing for the Negative Ions that they claim makes up “DNA” that move toward the Anode in Gel Electrophoresis. So to really walk through this, they are claiming to put “HIV” (A PCR positive cell culture) in a petri dish, they are then adding Metformin a drug which knowingly has Positive Charge and is highly attractive to H+ Ions due to its pH. They then test for its relative negative charge in PCR which tests negative.

To me this once again bolsters the hypothesis/point that all they are testing for is charge and given that this was carried out in concentration titers and it showed a sliding scale of efficacy this only cements that further. I want to go a bit further into my overall thinking, using the results of this experiment. It is something that I have thought for a while but haven’t really vocalized it, it is still a working hypothesis but I am confident enough to state that is what I think is going on: That all drugs are really very similar, certainly when it comes to drugs that are said to have any effects genetics. When you can use drugs like this, completely off target for the same purpose you do have to wonder. I think a lot of them are designed in the method of delivery and the way they are packaged to attempt to reach certain areas of the body for particular organ functions, but once again these are differences in essentially mechanical properties and how they are delivered.

Over and Out.

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