Emily O’Reilly: My brother’s HIV seemed under control. So why did he die?

Shortly after 8pm on May 29th, 2023, my brother Brian, aged 62, died at London’s Whittington Hospital. He had been admitted by ambulance late the previous night following a collapse at a nursing home.

At 11.40 that morning – observing his frailty – a doctor who did not know him advised against resuscitation should his heart stop.

“We like to have this conversation earlier rather than later,” she wrote in her medical notes, “and given his complex medical history, he is unlikely to benefit from CPR and [it] is more likely to cause more harm than good.”

[…]

Brian’s death certificate recorded the immediate causes of death; a pneumonia caused by food and liquid entering his lungs – and a “pseudo” internal obstruction.

As we know, pneumonia—and specifically, pneumocystis pneumonia (PCP), a fungal lung infection—was among the first five AIDS defining diseases. We will also see that Brian suffered from another AIDS defining illness, which is now acknowledged to be caused by a herpes virus, KSHV/HHV8—Kaposi’s sarcoma.

The underlying causes were: human immunodeficiency virus, the cancer Kaposi’s sarcoma (KS) and severe frailty.

By the time he died, Brian weighed just over eight stone, having lost four stone “unintentionally” in six months.

He had cachexia, wasting syndrome, his clothes loose around his body.

The russet lesions of KS – a cancer consigned in public memory to last-century deaths from Aids yet still recorded by the World Health Organisation as “Aids defining” – were visible on his legs, arms and chest.

Everything about this death – the virus, the cancer, the wasting – felt as though from another time.

I’m waiting until we get to the point that his treatment is described. It might provide some clue as to why he was so sick despite being on medication that allegedly kept his “HIV” at bay.

Brian had died more than 40 years after the western Aids epidemic began, more than 30 since his HIV diagnosis, a quarter of a century since effective HIV treatment had emerged.

It was so effective that he died despite it—or because of it?

Why then, at the end, did he look less like a survivor of the modern HIV era than a casualty of its first?

After his death, my conscious self split in two.

One part was a grieving sister, mourning the loss of a brother, friend, confidant, beloved of my children, his Christening my first conscious memory.

This must be very difficult and enraging for the survivors.

The other part was the curious professional – a former journalist, Ombudsman – wondering at the disconnect between the contemporary framing of HIV and my brother’s final two years and death.

His dying seemed impolite, offending against the narrative: that, with treatment, the crisis had passed, that people would live lives as long as anyone else’s.

But if that were true, how could someone whose HIV was well controlled by antiretroviral therapy die like this – in London – die in 2023?

How was it possible for someone to get KS on the very treatment that is meant to hold it in check?

How, indeed, was it possible? It’s almost as though “HIV” is irrelevant and that these illnesses were caused by something else entirely.

And if that cancer is – still – categorised as “Aids defining” – what did that mean in his singular case?

In a scant two years, Brian’s body had unravelled, developing cardiac, renal and liver failure alongside electrolyte instability that caused blackouts. A sling supported a shoulder fractured and repaired after a fall. Nerve damage to a foot confined him to a wheelchair. Chemotherapy in late 2022 weakened him; his body still dealing with the aftermath of intestinal surgery six years earlier, albeit successful.

I’d like to know if he was on Truvada, given the kidney and bone problems he experienced. I’m also curious about the “chemotherapy” he received. Was this to treat his KS?

Perhaps Brian’s history will help us understand how everything went so wrong.

Brian had emigrated to New York in 1982, aged 21.

[…]

As Brian planned his New York life – arriving at a peak of sexual freedom for gay men – a new threat was quietly announcing itself.

A June 1981 report from the Centres for Disease Control and Prevention described a rare lung infection, pneumocystis carinii pneumonia, in five gay men in Los Angeles. Two had died.

It was the first official report of what later became known as Aids. By 1995, one gay man in nine in the US had been diagnosed with Aids; one in 15 had died.

In 1990, Brian tested positive for HIV. Briefly returning to Ireland, he moved to London, remaining there with his partner for the rest of his life.

In 1997, the roll out of new antiretroviral drug regimens dramatically increased life expectancy. The terrors passed. He would live, but in a space that demanded vigilance, monitoring, blood checks, medication changes as side effects emerged – high cholesterol, anxiety, potential cardiac and kidney risks – 15 different antiretroviral therapy regimens between 1997 and 2022.

Finally we have the acknowledgment that the treatments themselves can be toxic, requiring constant monitoring and vigilance. It’s also unclear whether the author means that Brian himself received fifteen different treatments.

All of this – to me – was invisible. His chemical sentinels demanded attention, yet remained in the conversational shadows.

By the turn of the century, the HIV/Aids story was shifting. Online Aids memorials were less frequently updated; the remembered dead eternally stuck in the gay style subcultures of the decades they had died in.

HIV was there just as diabetes was or any chronic disease. Fewer people remembered the epidemic, even fewer its iconic disease – KS.

I trace the start of my brother’s decline to Easter 2021.

It came early that year. We met in London in late March. Walking down Euston Road, he was limping, his left foot dragging. En route to Sainsburys one day, he tripped. Passersby plucked him from the hedge he had tumbled into.

By the following summer he required a leg brace, ultimately, a wheelchair. An abnormal heart rhythm emerged in May; an attempted surgical fix failed two months later.

In September, his kidney function deteriorated.

His sodium levels fluctuated. He would faint, have seizures, attend A&E departments for sodium infusions.

This is sounding more and more like the treatment was worse than the disease. Had Brian exhibited any AIDS like illnesses prior to his starting ARVs? Read on.

Brian coped, using a spreadsheet to monitor test results, track appointments, forward emails, corral his siloed consultants.

I hovered as he shared the latest, speculative, diagnoses of his doctors; spinal cancer, breast cancer, motor neuron disease.

In March 2022, an older, more terrifying world returned. Lesions on his knee and ankle had concerned his GP, a biopsy to check for KS was planned. His HIV consultant said KS was “highly unlikely”. The markers of his immune defence were normal, his viral load undetectable.

Days later, a biopsy confirmed the cancer.

Allow me to remind you that KS is a very curious phenomenon that might, ironically, demonstrate that “HIV” is not necessary for AIDS.

He had options. This form of KS might remain on the skin and not spread into organs. He could die with it, and not because of it.

Brian did not want it, period. He craved chemotherapy, terrified of facial lesions. In a hospital day room one morning, he watched as people received intravenous chemotherapy.

I envied them, he said.

My brother was not a child of the 21st century with its optimistic HIV narrative, with Aids at least tamed – not even called Aids any more – but rather “advanced HIV” and everyone expected to live long and healthy lives.

Brian was a child of the 1980s western Aids epidemic, when tens of thousands of gay men died and the lesions of KS did more than signal illness. They marked you.

Four rounds of chemotherapy later, bruised from another fall, his treatment was stopped. Some lesions had faded; fresh ones arose on his legs, arms and chest.

So the chemotherapy was for KS.

The spring of 2023 brought more weight loss, more falls, a medication list so long, that in itself – “polypharmacy” – carried the weight of a separate illness.

A shoulder break required an operation and physiotherapy that he was too weak to endure.

He took vitamins, painkillers. He carried from hospital to home and later to care home a plastic bag filled with liquid food supplements. Medical notes suggested that he swap strawberry flavour for chocolate.

Brian had worked for a global corporation. In 2022, no longer able to do so, he lost his job and his health insurance, moving from private rooms, bespoke menus and – in one hospital – views of the playing fields of Harrow – to the chaos of overcrowded NHS wards and finally to a nursing home from where he was brought, on an early summer’s night, to Whittington Hospital to die.

Eight days after his death, the nursing home, in an email, attached its condolences to an unpaid bill.

Following his funeral in London, my brother, sister and I – a cat’s cradle of hands beneath the casket – placed his ashes in our parents’ grave.

I looked for answers to his death, to those final, brutal, two years, to the inability of myriad specialists to identify a unifying “why” or to keep him alive.

I searched for a missed diagnosis, an overlooked infection, a hidden cancer that might explain the catastrophic failing of his body.

But no explanation was forthcoming.

As administrator of his estate, I had access to his medical records.

Thousands of pages – unredacted – landed in my inbox. Over months, I studied them, rabbit holes of detail charting the minutest of procedures; the raising of a bed rail, the administration of a single tablet, the subdivision of a daily calorie intake.

Occasionally, one could sense someone standing back, observing this cascade of illnesses, marvelling at their profusion, musing about HIV, the possible spread of KS, inter-organ damage, undetected other cancers, one medication interfering with another, the notes littered with upside down question marks, the medical shorthand of perplexity.

His emotional state was noted. “Patient visibly anxious”, “frightened”.

Well, of course he was anxious and frightened. According to the AIDS establishment, he was doing everything right, being compliant to his treatment and attending to the numerous side effects with treatment for them as well. No wonder the poor man was terrified.

Obtaining his HIV clinic notes continued to prove difficult, the illness still carrying layers of privacy and protection and shame.

I met his HIV consultant. He asked if a student could attend as he, the student, “hasn’t done one of these before”.

The student – younger than my son – was already in the room, my dead brother and I now a teaching moment.

A “constellation of medical problems” had led to Brian’s decline and death, the consultant said. His deterioration was very apparent, but it was “hard to label him as terminally unwell”.

The emergence of KS was an “unexpected and very unusual scenario” for someone undetectable with a good CD4 count – a key indicator of immune system health – for so long.

As we know, KS has been observed in “HIV” negative people and now, in a patient with undetectable viral load and a healthy T cell count. Read on, though—we shall see an interesting connection to a phenomenon we have discussed here before, and that is accelerated aging.

Listing Brian’s illnesses, he said none were linked to HIV, concluding that while HIV and KS were “mentioned” on his death certificate, they had not been “major players”.

I understood the clinical distinction; HIV did not directly cause Brian’s cardiac, kidney and other system failures as once it had caused normally quiescent infections to run amok, yet the attempt to detach Brian’s death from the virus he had lived with for 33 years, jarred.

So, somehow “HIV” didn’t manage to cause this man’s total immune collapse, yet he supposedly had “HIV” AND AIDS. These are some mental gymnastics we’re engaging in here.

I turned to medical literature, using search terms that might give coherence to medical incoherence. What emerged was something less tidy, less clear cut, the possibility that there was no single explanation at all.

Paper after paper described “premature frailty”, “multi-system illness”, “wasting”, “polypharmacy”, the earlier onset of diseases associated with ageing despite effective HIV treatment.

Brian ticked every box.

His consultant had told me, “… ageing in people who have had HIV for a long time is an emerging topic that we are still learning about”.

I encourage you to read my post on “HIV” positivity and accelerated aging. Is it caused by the drug regime? One wonders.

A lot of people, it appeared, were doing so. In 2021, as Brian’s illnesses began to gather, The Lancet medical journal – in the first of a series of papers on ageing with HIV – had noted that prolonged survival with HIV translates – even on antiretroviral therapy – into an “increase of non-Aids-defining illnesses associated with age”.

But Brian’s illnesses—pneumonia and KS—ARE AIDS defining illnesses. This is really quite incredible an attempt to claim this man did not suffer from massive immune collapse—after all, he was medicated and presumably undetectable—his having AIDS surely is an inconvenient truth.

The terms “accelerated ageing” and “accentuated ageing” recurred across the literature, with calls for the greater integration of the science of biological ageing with HIV care.

We have discussed accelerated aging before.

What had happened to Brian was hiding in plain sight; his biological clock appeared to have detached from his chronological age.

The old epidemic had changed tempo but Brian’s generation of people with HIV had had to age before science could see that, to see clinically what ageing with HIV looked like.

But if his virus was suppressed and he had a healthy level of T cells, what was causing the accelerated aging, since “HIV” cannot be the culprit if it’s suppressed, per the mainstream. It’s not just me saying this.

It was one thing to examine cells under a microscope, another to see a hypothesis played out in a human being many years later.

Brian’s generation had lived through the uncontrolled first encounter with the virus, through successive generations of treatment, surviving into middle age many years after the epidemic’s peak.

The treatments extended life dramatically, but many early regimens carried toxicities that became fully visible only over time.

Finally we have the truth bomb—these medications are not as simple and happy as we are led to believe. For every patient who claims that their diagnosis is “nothing” when treated with ARVs, we have several whose bodies have been decimated by the drugs. Recall the 26,000 Truvada plaintiffs, whose kidney function and bone density have been compromised, sometimes permanently.

HIV had not produced the catastrophic immune collapse associated with the epidemic years, but decades of immune activation, illness and treatment perhaps exacted a slower, cumulative, price.

The role of KS in Brian’s death remains unresolved. It did not appear to be the aggressive KS of the epidemic years but nor did it appear to be the slower moving “classic” KS.

Perhaps we haven’t solved KS, and therefore AIDS, because we are barking up the wrong tree with “HIV?” Could the activation of KSHV hold some clues?

Nothing else had been found to explain the wasting that had consumed him.

No one said, “this is what he needs to get better”.

Interventions were reactive, fragmented: sodium levels corrected, falls treated, scans ordered. Each intervention made individual sense, collectively they mirrored the dissonance of his decline.

My brother has now been dead for three years. I have found no simple answer to the question I had asked then: how do you die like that when the dominant post-crisis consensus suggests that people on effective HIV treatment are no longer expected to die this way?

What I found instead is that ageing with long-term HIV can look like this for some of the first western epidemic generation: not one catastrophic opportunistic infection, not the old Aids deaths of the 1980s and 1990s, but rather an accumulation of frailty, inflammation, malignancy, organ damage, medication, fear and exhaustion.

My brother’s story had not been drawn from an older playbook. It was not out of date, not an outlier, not drawn from an obsolete HIV past.

It was, rather, recognisably contemporary.

I am really sorry that this man was so failed by the medical system, and I am sorry for what his surviving family members are going through. They must be internally screaming with frustration.

I do wish more information had been given as to what medications he was on and his surrogate markers of T cells and viral load; the context of the article certainly indicates that his markers were normal.

However, this case study ought to serve as a cautionary tale. An “HIV” diagnosis is dangerous not because it might lead to AIDS, but because it retains people in care using treatments that cause not only kidney failure, bone density loss, liver damage (in the early days of the protease inhibitors), metabolic issues such as lipodystrophy and elevated cholesterol, but also massively accelerated aging, despite the total suppression of “HIV.” An urgent reckoning is far overdue on the true causation of AIDS, and if this does not happen sooner than later, we will see many more Brians moving forward. Never again.

All of that was true before AI swept into, it seems, every industry on the planet. Are preapprovals—for medications, outpatient procedures, inpatient surgery, in-home healthcare and a multitude more—about to exit the realm of human decision making because it’s faster and less expensive to design an AI program to do it?

That’s the question recently explored by MedPage Today’s N. Adam Brown.

“The U.S. healthcare system has officially entered the era of artificial intelligence (AI). Organizations, practitioners, and patients are no longer merely trying on a new fad, they are operationalizing the tool,” Brown reported. “...In doctor’s offices and hospitals, AI is used to write notes, triage messages, predict readmissions, summarize charts, suggest differential diagnoses, and even to make prescription decisions that, previously, a physician would have made.” (1)

Now, whether you love your doctor or barely tolerate him/her, a physician can take human situations under consideration when making treatment decisions.

And if you have a difficult-to-diagnose or treat illness like ME/CFS—or if you’ve been diagnosed as HIV-positive but aren’t down with taking the toxic cocktail du jour—you might be lucky enough to have a doctor who understands.

Does Dr. AI possess the same sensibilities?

While AI in the doctor’s office is helping reduce paperwork overload, allowing more patients to be seen while reducing “clinician burnout,” doctors are beginning to worry that decisions by insurers—particularly prior approval decisions—are already being made by machines without any human input.

“They are right to worry,” according to Brown. “In some reported cases, denial decisions were processed at a speed that makes meaningful physician review unlikely.” (1)

Is AI an important and helpful tool in doctors’ offices? The answer is often yes.

“The core issue is not that AI is being deployed in healthcare settings,” Brown pointed out. “It is how it is being used. There is a fundamental difference between viewing AI as a tool to enhance human skill and knowledge and using AI as a gatekeeper for care.

“A tool supports human judgment. A gatekeeper replaces it.” (1)

Fortunately, doctors’ associations like the AMA, governmental agencies like the Centers for Medicaid and Medicare (part of HHS), are demanding “greater oversight of insurer AI use, emphasizing transparency, bias mitigation, and the need for human review in decisions that affect patient care.” (1)

And what can patients do if they feel the wrong decision has been made by the insurer, possibly by an AI algorithm instead of a physician?

Enter the lawyers.

Unfortunately, the law around AI’s technological advances is still somewhat murky.

As David S. Greenberg wrote on ASFlaw.com, “The question is whether health insurers are using their AI predictive tools properly, in accordance with state and federal law, or whether they are being deployed solely as cost-saving measures to improperly deny patients and health care providers coverage and payment for medically necessary services.” (2)

Both Cigna and United Healthcare (UHC) have been sued by families or groups of patients who suspect that a machine made crucial healthcare decisions that resulted in death or disability, overriding the patients’ physicians.

In the Cigna case, “The plaintiffs accused Cigna of relying on the AI algorithm [named “PXDX”] to enable its own doctors to automatically deny thousands of claims at a time for treatments that did not match certain preset criteria without actual physician review of the medical records.” (2)

The UHC lawsuit involved two deceased patients.

“The plaintiffs allege that UHC improperly used the nH Predict AI Model to deny extended care claims for elderly patients based on erroneous health care determinations generated by the algorithm. The plaintiffs also accused UHC of using the AI tool to override the determinations of medical professionals, including ones employed by the insurer.” (2)

But will increasing numbers of such lawsuits be successful?

In MedPage Today, Brown wrote, “Accounting for these realities is one reason the legal framework for AI has not caught up to the technology. As discussed in recent academic work, including analysis from Harvard’s Petrie-Flom Center, liability in the age of AI is deeply uncertain because traditional models of malpractice assume a human decision-maker. AI eliminates that feature.” (1)

And with human decision-making eliminated, Brown asks, who is accountable when things go wrong?

BIBLIOGRAPHY
1. N. Adam Brown “Is AI Healthcare’s Newest Bureaucrat?” MedPage Today, 5/12/26. https://www.medpagetoday.com/opinion/prescriptionsforabrokensystem/121230
2. David S. Greenberg. “Intelligence to Decline Medical Claims.” December 22, 2023. AFSlaw.com. https://www.afslaw.com/perspectives/health-care-counsel-blog/health-insurers-sued-over-use-artificial-intelligence-deny

Queer men's obsession with 'PrEP belly' indicates that our priorities might be a little skewed

If you’re chronically online, you’ve probably heard the term “PrEP belly” emerge from the image-obsessed corners of the gay wide web.

For the uninitiated, PrEP (pre-exposure prophylaxis) is a highly effective medication that helps prevent HIV infection in at-risk populations. One of the most important public health tools in modern history, PrEP dramatically reduces transmission rates of a virus that devastated generations of LGBTQ+ people. I take it every day.

We have the mandatory ode to PrEP. “I take it every day.” This entire piece takes way too long to tell us that AIDS was bad & the only way to stop it is to take PrEP. Why, again, are people clamoring for the government to pay for drug to treat a disease they don’t even have?

Also, this wording is very odd. Why do they say that PrEP helps in “at risk populations?” Does it not help in non risk groups, as it should if it is truly effective? I mean this question sincerely; it’s a very weird statement when you think about it.

At the height of the AIDS crisis — which wasn’t that long ago, by the way —hundreds of thousands of people in the U.S. alone died from HIV-related illnesses. But now, just a few decades later, a new (albeit far less nefarious) panic has emerged: the belief that taking PrEP could give you a potbelly.

The rumor seems to have gained traction after a social media comment claimed that celebrity DJ John Summit had “PrEP belly,” according to Them. From there, the problematic discourse swelled and mutated. Gay men across TikTok and X were scrutinizing their stomachs, wondering whether the medication protecting them from HIV was also making them unsexy.

Medical professionals have overwhelmingly agreed that excessive midsection fat is not a common side effect. Some people may experience temporary bloating or digestive discomfort when they first start taking the medication, but these symptoms are generally mild and last only a few days to a few weeks.

“One area of ongoing discussion is weight gain, and abdominal weight gain in particular, associated with PrEP,” says Dr. Isaac Dapkins, internal medicine HIV specialist and chief medical officer for the Family Health Centers at NYU Langone. “Earlier studies of TDF/FTC [the earlier version of PrEP, known best as its brand name Truvada], including the iPrEx metabolic substudy, suggested that this form of PrEP may have a modest weight-suppressive effect.”

So they’re deliberately obfuscating here. They refer to Truvada, or TDF, as being this drug that can help you lose weight—but that is not the drug under consideration here; the drug that allegedly causes “PrEP belly” is a different medication. Why mention the other drug at all? It’s irrelevant.

I wonder if more people would be rushing to take it if they knew about that potential side effect.

Dapkins, however, says that this potential weight loss is largely viewed negatively because it may have resulted from mitochondrial dysfunction. Mitochondria, you might remember from junior high chemistry, are part of our cells that produce energy. We don’t want that depleted.

More recent studies that tested newer PrEP agents did so in comparison to TDF/FTC, he says, and did find the potential for minor weight gain as a side effect — but some of this difference may reflect the absence of the previous version of the drug’s weight-suppressive effect.

“In addition, observed weight gain with newer agents may be similar to weight trends seen in comparable populations not receiving PrEP, although some groups, including women and non-white patients, may experience greater changes,” adds Dapkins.

Overall, it appears that “PrEP belly” panic might be an overreaction. Still, the panic itself says something darker about where we are culturally as gay men. Gay culture has always revolved, in part, around visibility and ***, but somewhere along the way, it feels like health (and being nice to each other) started becoming secondary to aesthetics. We’re beginning to lose the plot, and as silly as “PrEP belly” is, it does point to a murky issue in our community.

What on earth are those *** intended to mean?

What makes the “PrEP belly” discourse feel especially bleak is the historical amnesia underneath it. Now that we have the tiniest amount of distance from the HIV epidemic, we’re treating HIV prevention as casual lifestyle branding rather than the extraordinary medical breakthrough it actually is.

And yet the fear of maybe gaining a little stomach fat was enough to send parts of the internet into a panic. And trust me, I understand the impulse and I’m not immune to it, either. Gay men are constantly told, both implicitly and explicitly, that our value is tied to how successful, desirable and optimized our bodies appear. But misinformation around PrEP has real consequences and even joking rhetoric can discourage people from taking medication that could quite literally save their lives.

Women, as well as gay men, are told that our value is tied to our bodies, as well. It is a really hard thing to navigate.

“For many patients, the substantial reduction in HIV transmission risk will outweigh the potential concern about weight gain,” says Dapkins, adding a disclaimer of nonjudgment, “but this should be reviewed thoughtfully between the patient and clinician.

More than anything, the “PrEP belly” conversation reveals how distorted some of our priorities have become. A generation ago, queer people would have done almost anything for access to medication this effective, and many risked their lives protesting a government that cared little that gay people were dying in droves. Today, some people are afraid to take it because they think it might blur their abs. I think as a community, we can and should do better.

I don’t know what to say about this. Maybe it’s correct to infer that an adverse effect like weight gain might indicate a deeper medical problem, and that these people are correct to be concerned. Regardless, I wonder how long it will be until there are lawsuits on “good Truvada,” as well.

Drug Resistance and Novel Antimicrobial Agents Challenges facing long-acting PrEP implementation in large populations

Let’s dive in.

The introduction of long-acting antiviral prophylaxis drugs, exemplified by the twice-yearly injectable capsid inhibitor lenacapavir, marks a remarkable advance in HIV prevention, which addresses the adherence issue that has limited the real-world use of daily oral pre-exposure prophylaxis (PrEP). The long-acting formulations of lenacapavir offer a potent prevention tool, particularly well-suited for countries where the HIV transmission mainly occurs in certain populations with high incidence.

Their reasoning makes sense at first glance, but read on. There are plenty of potential problems with this strategy.

This pharmacological strategy, while powerful, still faces challenges, including the inherent limitations that constrain the use of drugs to prevent large-scale human transmission of viral endemics such as HIV. First, its mode of action – direct pharmacologic inhibition of viral replication – confers no immune memory, and its protection efficacy is exclusively contingent on maintaining therapeutic drug concentrations above a critical threshold.

So, it’s a preventative that works by inhibiting viral replication? These people don’t HAVE the virus, so what is being inhibited here? Is the idea here that people actually DO get infected on this drug, but the virus is rapidly cleared? Papers describing the trials for these drugs don’t make this clear.

This necessitates lifelong administration at strict, regular intervals (e.g., every several months), leading to a number of consequences. Second, the immediate consequence is cost. At current prices of $28,218/person/year in the US market, a single person will cost $1,693,080 (assuming 60 years of taking the medication every 6 months).

• Every six months for SIXTY YEARS? That’s pretty amazing—they assume people will be on these drugs for literally a lifetime, say from 20 to 60? All for a disease they don’t even have? And the price tag—wow.

It is crucial to acknowledge that Gilead Sciences has announced voluntary licensing agreements aimed at supplying generic lenacapavir to high-incidence, resource-limited countries, but it is still a significant healthcare cost to any country without a rich healthcare budget. Third, this brings a significant public health challenge in many generalized epidemic countries or regions; HIV transmission does not just happen in certain populations with high incidence. While populations with high incidence account for 55% of new HIV infections globally, a substantial 45% still emerge within the broader general population. This implies that the drug prevention approach has to apply to the entire population to achieve epidemic control.

Let me translate this for you. Since “HIV” transmission in certain countries occurs largely in the general population, selling these drugs only to risk groups will likely prove ineffective, so we need to be injecting the general population. This doesn’t seem feasible to me, especially given the financial cost of these drugs—they aren’t cheap, as described in this article.

Fourth, the requirement of country wide participation not only further multiplies the cost of the entire programme but also generates systemic challenges on how to implement such a large and complicated drug intervention programme for everyone in the country. For instance, in resource-limited settings, the lack of accessible clinics, transportation barriers for rural populations, the necessity for cold-chain supply management, and the severe shortage of trained healthcare workers will severely limit consistent adherence. People need to seriously consider who can administer such large-scale, drug-based HIV prevention programmes and where the money is to support such health delivery and management operations. Thus, achieving improvements in these regions would necessitate massive international funding and parallel investments in primary healthcare systems, rather than a singular focus on drug itself.

This all sounds very tenuous.

Notably, this drug prevention approach carries a non-negligible and evolving biological risk – the selection for drug resistance. To rigorously evaluate this challenge, it is essential to distinguish between the current baseline status of primary drug resistance (PDR) and the potential risk of acquired drug resistance (ADR).

I can imagine that after sixty years, resistance might well develop. This is utterly ridiculous.

Recent large-scale epidemiological surveillance indicates that the natural resistance rate to lenacapavir is currently extremely low globally. For instance, a global analysis encompassing 85 countries and over 50,000 sequences demonstrated an overall lenacapavir resistance rate of 0.31%, and studies on the Chinese population reported a PDR rate of 0.17% among treatment-naïve individuals. This exceptionally low baseline of natural resistance actually provides a highly favourable window of opportunity to support the large-scale initial rollout of the drug. Nevertheless, the threat of ADR remains a critical concern. The resistance frequency for HIV drugs can escalate rapidly, particularly in scenarios of undiagnosed acute infection at initiation or suboptimal adherence to the injection schedule.

Oh, there it is—“undiagnosed acute infection at initiation.” That’s a loophole they use constantly. I have a question. Why can’t they FIND “HIV” at acute infection? You’d think that with the body teeming with the virus, this would be easily accomplished without resorting to PCR to magnify viral fragments, but as far as I know, even PCR isn’t used to diagnose “acute infection.” This is some top level gaslighting happening with “acute infection.” Also, “suboptimal adherence to the injection schedule?” More gaslighting again—if things fail, it’s the patient’s fault for not being appropriately adherent.

The recently confirmed emergence of lenacapavir-resistant variants in clinical settings validates this ongoing threat. Therefore, we must utilize the current window of low resistance to promote the drug while simultaneously establishing robust global surveillance systems and strict adherence management protocols. Without such safeguards, the widespread use of a single-agent, long-acting prophylactic could inadvertently drive the population-level selection of resistant virus strains, thereby compromising the efficacy of not only prevention but also therapeutic options for patients infected with multidrug-resistant HIV strains.

What do you want to bet lenacapavir is going to fail on a population level, and resistance will be blamed? What is then the next step? Regardless, the rollout continues, but the search for a vaccine soldiers on, because we need every kind of preventative, apparently.

Most critically from a public health perspective, the protective scope of long-acting prophylaxis drugs is inherently confined to the individual level. It functions as a personal shield rather than a community-wide intervention, especially focusing on identified groups with high incidence. While this targeted approach is vital, it cannot generate herd immunity and does not reduce the basic reproduction number (R₀) of HIV across a general population.

This paragraph attempts to explain why the development of a vaccine is crucial—the injectables don’t provide “population level” protection; they cannot reduce the basic reproductive ratio, which is not well defined for “HIV.” So the search for a vaccine continues, over forty years after it was begun. I’m not holding my breath.

In contrast, a successful preventive HIV vaccine will provide sustainable and population-wide epidemic control. The induction of specific immune responses, aiming to establish the host’s long-lasting immune memory, potentially confers protection for years or even for decades following a few doses of vaccinations. However, it is important to objectively note that a future vaccine will present its own logistical challenges. Equitable global distribution, stringent cold-chain management, and the requirement for trained personnel to administer the immunizations remain significant hurdles that must be addressed even after an effective vaccine is developed.

You have to love their optimism, after nearly every vaccine trial has been abandoned for futility. There are no indications that this will change.

The development of an HIV vaccine remains a persistent challenge, largely due to the virus’s high genetic variability and heavily glycosylated antigens, which collectively facilitate immune evasion. Furthermore, this difficulty is compounded by the lack of reliable animal models, the absence of well-defined correlates of protection, and the significant ethical and biosafety concerns that complicate clinical trials. An effective HIV vaccine remained elusive despite decades of intensive research. However, recent scientific advances have provided encouraging signs of hope. Novel approaches, such as germline-targeting strategies aiming to elicit broadly neutralizing antibodies (bnAbs) and the development of polyvalent DNA prime-protein boost HIV vaccines (PDPHV), are currently being validated in early-phase clinical trials and represent critical breakthroughs.

I appreciate that they acknowledged the lack of an animal model for “HIV.” If you were around during Peter Duesberg’s criticisms, you know that monkeys have been injected with “HIV,” develop immunity in the form of a positive antibody test, but stubbornly refuse to develop AIDS, or even “HIV disease,” whatever that is.

In any case, what we can not do is to use the progress of drug prevention as a reason for stopping HIV vaccine development. Significant progress in long-acting HIV prevention drugs has positively impacted prevention efforts, and this approach has not superseded vaccine development; rather, both should hold continued and complementary value. The choice is not a binary opposition between drugs and vaccines.

Of course we need both!

Preventive HIV vaccines remain the optimal solution for herd immunity, and long-acting PrEP drugs can serve as a vital bridge and an individual-level shield, particularly for groups with high incidence. To achieve the 2030 goal of ending the AIDS epidemic, a combination prevention strategy is essential (Figure 1). It should integrate timely testing and diagnosis (voluntary counselling and testing (VCT), HIV self-testing, etc.), behavioural interventions (condom promotion, peer education, etc.), biomedical interventions (long-acting PrEP, post-exposure prophylaxis (PEP), etc.), and ongoing research into HIV vaccines and cures. Ultimately, these tools serve as complementary, synergistic components of a comprehensive public health response.

Well, this article limps to a finish. We have four years—less, really—until 2030. What do you think the chances are that “HIV” will be extinct in 2030? I have a bridge to sell you if your answer is yes.

As always, let me know what you think in the comments below.

In the Groundhog Day miasma that surrounds ME/CFS and HHV-6 research, an international team of scientists just discovered this decades-old finding all over again.

Primary authors Stefan O. Ciurea (University of California, Irvine, USA) and Piyatida Chumnumsiriwath (Naresuan University, Phitsanulok, Thailand) and team published their findings in the February 2026 supplemental issue of Science Direct, “Transplantation and Cellular Therapy.” (1)

The type of transplants they studied retrospectively was called “allo-SCT,” which is short for allogeneic stem cell transplant. (Unlike “autologous” transplants, which use a patient’s own cells, “allogeneic”—i.e., allo-SCT—transplants use healthy stem cells from a matched donor.)

“Reactivation of human herpesvirus 6 (HHV-6) is common after allogeneic stem cell transplantation (allo-SCT) and has been associated with worse transplant outcomes,” Ciurea and colleagues reported. “In a previous study involving a small patient population, we observed that preemptive therapy with once-daily foscarnet at doses of 60-90 mg/kg/day for 7 days (FCN) resulted in rapid viral clearance, potentially reducing HHV-6-related complications.” (1)

This second 2026 study involved more patients, they pointed out:

“We retrospectively analyzed 138 consecutive adults (≥18-year-old) who underwent allo-SCT at our institution between 05/2020-06/2025. Plasma HHV-6 viral load was monitored utilizing quantitative PCR twice monthly during the first 100 days post-transplant. All patients with HHV-6 reactivation received FCN as above, with viral load monitoring at least twice weekly until clearance.” (1)

“All patients responded to treatment,” according to Ciurea and team; “3 patients (8%) developed recurrent HHV-6 reactivation, all responsive to retreatment.” (1)

Furthermore, all patients had successful transplants “without secondary graft failure.”

Most importantly: “No encephalitis or pneumonitis occurred after treatment. Two patients developed acute kidney injury (5.4%) grade III which resolved after hydration.” (1)

In other words, they had a 100% success rate when they treated transplant patients with foscarnet.

In 1993, I interviewed Dr. Konnie Knox, who was then a cancer researcher in the Immunotherapy Program at St. Luke’s Medical Center in Milwaukee, Wisconsin. At that time, she and colleague Dr. Donald R. Carrigan were examining the role played by HHV-6 in not only cancer but also in organ transplantation. Knox and Carrigan were looking for treatments that would halt the damage inflicted by HHV-6 in AIDS, ME/CFS, and transplant patients. HHV-6, Knox explained, “can infect the brain, the lungs, the lymphoid organs, and the bone marrow.” (2)

In a research paper they’d just published, Knox and Carrigan had examined HHV-6 multi-organ system infections. “Which antiviral drugs have effectiveness against HHV6-A? We know that foscarnet does; we know that ganciclovir does; and we have treated patients with those agents. We have specifically treated HHV-6A infections with foscarnet and seen very nice reversals of clinical syndromes.” (2)

Knox and Carrigan’s findings were not unique even in 1993. Among other teams examining the incidence of HHV-6 in organ transplant patients were Dr. Richard Cone and colleagues in Seattle. They published an analysis of HHV-6 in pneumonitis and graft-versus-host disease (GVHD) in bone marrow transplant recipients. (3,4)

Graft-Versus-Host Disease (GVHD) is a potentially life-threatening illness that strikes bone marrow transplant recipients. In GVHD, the donor’s healthy T-cells (which are impaired in AIDS and ME/CFS) attack the recipient’s tissues; GVHD is a form of organ rejection. The symptoms of GVHD include fever, rash, hepatitis, diarrhea or abdominal pain, vomiting, and weight loss. In 1993, it was found that HHV-6 was also causing pneumonitis, an often-fatal lung illness that can occur following bone marrow transplantation. (3)

In the Seattle study, some of the bone marrow transplant patients who developed pneumonitis caused by HHV-6 also developed severe GVHD. Those patients were found to have very high levels of HHV-6, particularly in their lungs. (3)

So the question arises: Who is—and who’s not—receiving foscarnet (or ganciclovir) to treat the HHV-6 infections we know are found not only in transplant patients but also in ME/CFS and AIDS patients?

It’s true that no treatments have been FDA approved for ME/CFS (and also that most approved AIDS medications and preventatives are highly toxic). Why aren’t physicians prescribing foscarnet and ganciclovir (and any other effective antivirals) as off-label treatments for patients with detectable HHV-6 infections who aren’t transplant patients, no matter what their diagnoses?

Off-label prescribing is all the rage all over the world: approximately 21% to 25% of “all prescriptions in general outpatient settings are for off-label purposes. For anti-infective medications, which include antivirals and antibiotics, the rates are significantly higher, particularly in specialized or high-risk settings.” (5)

Those high-risk settings include hospitalized children: 60.6% of antimicrobial (antiviral and antibiotic) prescriptions in pediatric wards are off-label. In adult Intensive Care Units, the overall off-label prescribing rate ranges from 25.4%
to 43%, “often driven by a lack of alternative approved treatments for critically ill patients.” (5,6)

BIBLIOGRAPHY
1. Piyatida Chumnumsiriwath, Stefan O. Ciurea, et al. “Once-Daily Foscarnet As a Treatment Strategy for HHV-6 Reactivation after Allogeneic Stem Cell Transplantation.” Science Direct, Volume 32, Issue 2, Supplement, February 2026. https://www.sciencedirect.com/science/article/abs/pii/S2666636725024789
2. Neenyah Ostrom. “Dr. Konstance Knox Explains Why HHV-6 May be The Key to Dealing with AIDS.” Appendix A in America’s Biggest Coverup: 50 More Things Everyone Should Know About the Chronic Fatigue Syndrome Epidemic and Its Link to AIDS.” Amazon 2022. [First Published in the New York Native, issue #678, April 15, 1996]
3. Neenyah Ostrom. “HHV-6 Seems to Be Causing Lung Disease in Immunosuppressed Individuals.” Chapter Four in America’s Biggest Coverup: 50 More Things Everyone Should Know About the Chronic Fatigue Syndrome Epidemic and Its Link to AIDS. Amazon 2022.
4. Cone, Richard W. et al.; “Human Herpesvirus 6 in Lung Tissue from Patients with Pneumonitis After Bone Marrow Transplantation”; New England Journal of Medicine, July 15, 1993.
5. Off-label Prescribing Rates. Google AI.
6. Zichao Ji, Xin Wang, Jiawei Wang. “Analysis of off-label drug use and its influencing factors in pediatric patients undergoing otolaryngology, head, and neck surgery.” Front Pharmacol. 2025 May 30;16:1553221. doi: 10.3389/fphar.2025.1553221

FDA Approves New Standalone Combo Pill for HIV

Let’s dive in.

The FDA approved islatravir-doravirine (Idvynso) as a standalone, single-tablet regimen for treating HIV in virologically suppressed adults, Merck announcedopens in a new tab or window on Tuesday.

These drugs all have the weirdest names. So, what are islatravir and doravirine, anyway? We’ll get to that soon, but first, who is this drug intended for?

Approval stipulates use of the oral combination in patients with HIV-1 who are virologically suppressed on stable antiretroviral therapy (ART), have no history of virologic treatment failure, and have no known substitutions associated with doravirine resistance. Co-administration with other ART medications is not recommended.

So, if these patients are virologically suppressed and have not failed treatment, why are they being switch to this combination medication? Could it be the… adverse effects of the most popular anti-“HIV” drugs?

Two- and three-drug regimens with second-generation integrase strand transfer inhibitors (INSTIs), such as bictegravir, are standard in initial HIV therapy. However, some patients face INSTI resistance issues and contraindications.

In two phase III trials, switching to the INSTI-free single-tablet islatravir-doravirine therapy was just as effective at maintaining viral suppression as bictegravir/emtricitabine/tenofovir alafenamide fumarate (BIC/FTC/TAF; Biktarvy) or a previous ART regimen for virologically suppressed HIV-1 patients.

Ah, we’re getting some answers now. People are experiencing resistance to integrase strand inhibitors (INSTIs), so the clinicians want to try an INSTI-free regimen for these patients. Also—contraindications? What contraindications, exactly?

“Idvynso is the first non-INSTI, tenofovir-free, two-drug regimen to demonstrate noninferior efficacy to standard oral antiretroviral regimens, including Biktarvy,” investigator Amy Colson, MD, director of research at Community Resource Initiative in Boston, said in a statement. “This makes Idvynso a potential alternative for people with virologically suppressed HIV who may need to switch their treatment.”

Read that paragraph carefully. This new drug is being advertised as “tenofovir free.” As we know, tenofovir based drugs are associated with severe, sometimes life threatening adverse events, with both their TDF (“bad Truvada”) and TAF (“good Truvada”) formulations. Is this the impetus behind the production and approval of this drug?

Islatravir is a nucleoside analog reverse transcriptase inhibitor that blocks HIV-1 replication by multiple mechanisms. Doravirine is a non-nucleoside reverse transcriptase inhibitor that binds to and blocks HIV reverse transcriptase; the drug was first approved in 2018 under the brand name Pifeltro.

So islatravir is a nucleoside analogue RT inhibitor (NRTI) and doravirine is a non-nucleoside RT inhibitor (NNRTI), which means that these drugs terminate DNA synthesis and effectively kill cells. They are the oldest type of ARV, AZT is an NRTI. So they’re recycling all this old drug technology, and moving people from one medication regimen to another as soon as either “resistance” or adverse events rear their ugly heads. This new drug better be great… oh, wait.

In the two trials, 1.4% to 1.5% of patients switching to islatravir-doravirine lost viral suppression (≥50 copies/mL of HIV-1 RNA) at 48 weeks compared with 0.6% and 4.9% of those who took BIC/FTC/TAF or remained on a previous ART regimen, respectively. Islatravir-doravirine users had minimal weight changes from baseline in both trials.

So basically there is nothing special about this drug. I can only speculate as to what reasons there might be to push this new drug, and the options are not good. Why introduce yet another variant of the same old, toxic drugs?

And what about side effects of this drug?

Common adverse events reported in the islatravir-doravirine arms of the trials included diarrhea (1-3%), dizziness (1-2%), fatigue (1-2%), abdominal distension (1-2%), headache (1-2%), and increased weight (<1% to 2%). Merck also noted a single case of severe immune thrombocytopenia that started a month after treatment initiation but resolved after stopping therapy.

Resolved after stopping therapy. Let that sink in. How many individuals were enrolled in this trial?

Islatravir is the anchor medicine in other investigational two-drug combinations being developed as potential once-weekly treatments for HIV.

It’s also possible that this drug is being pushed because it has potential for less frequent dosing compared with one pill a day.

Warnings and precautions in the labeling notes severe skin reactions, including Stevens-Johnson syndrome/toxic epidermal necrolysis, and drug rash with eosinophilia and systemic symptoms.

Islatravir-doravirine is contraindicated with strong CYP3A enzyme inducers or the ART drugs lamivudine and emtricitabine.

Stevens-Johnson syndrome is nasty. Also, eosinophilia and “systemic symptoms?” This drug sounds like yet another nightmare marketed to “risk groups.” Pardon me if I’m suspicious.

In addition to immunotherapy and a “DNA vaccine,” the UCSF clinical trial employed a technology named “electroporation,” which Perrault was told by his medical team would feel like a punch in the arm.

Here’s how Perrault described the experience to Mohney:

“So I go in, I’m a little cavalier about it,” he told SFGATE. The medical
team held him down on the exam table, startling him, before giving him
an electric jolt and a type of vaccine called a DNA vaccine simultaneously.

“I screamed,” Perrault recounted. “I’m like, ‘That was not a punch, that
was an electric shock, people!’ ”

Unfortunately for Perrault, the procedure had to be immediately repeated
in his other arm.

“I started trembling. I’m like, ‘That was bad, that was scary,’ ” he recalled.
The researchers warned Perrault he would need another round of
electroporation in a few weeks. (1)

Dr. Steven Deeks, a professor of medicine and an “HIV expert” at UCSF, designed and led the clinical trial at sites in ten states and Puerto Rico. (2,3)

“They created a three-pronged approach to the immunotherapy treatment after being inspired by three different primate studies,” Mohney reported in SFGATE. “Normally, when a person with HIV stops taking their ART medication, the virus rebounds in a matter of weeks. The researchers hoped to retrain the immune system of HIV patients to keep the virus at bay without medications for a longer period of time.” (1)

Their 2025 publication, Deeks and colleagues explained, was “modeled after strategies that demonstrated positive effects in non-human primate (NHP) models ... we conducted a three-stage study in ten people living with HIV on suppressive ART involving (1) therapeutic vaccination with an HIV Gag conserved element (CE)-targeted DNA/MVA regimen to enhance HIV-specific T cell responses; followed by
(2) a combination of two relatively long-acting bNAbs ... and a potential latency reversal agent ... during ART suppression to reduce the size of the HIV reservoir; and finally (3) administration of the bNAbs immediately before pausing ART and undergoing analytic treatment interruption (ATI) to potentiate host immune responses by slowing rebound and/or possibly inducing the vaccinal effect.” (2)

[If you’re particularly interested in the pharmacology of this clinical trial, I encourage you to read this open access paper in Nature, reference #2 below.]

So, let’s break this down a little further.

Each of the ten participants was on “suppressive” ART (antiretroviral therapy) at the beginning of the study. ART, as you may know, is a pill or injection that patients are instructed to take daily, or sometimes weekly, for the rest of their lives. (2)

Like the drugs used for PrEP, antiretroviral drugs can have serious, even toxic, adverse effects ranging from fever, rash, nausea, diarrhea and vomiting to impaired cognition, depression, psychosis, kidney failure and more. (4)

The clinical trial’s “three stages” described by Deeks et al. above were, to simplify: a “therapeutic vaccine,” a TLR (toll like receptor) agonist, and bNAbs (broadly neutralizing antibodies).

The therapeutic vaccine used in this study was “an HIV Gag conserved element.” As the protocol on ClinicalTrials.gov explains, it aspired to test the “efficacy of a novel vaccine encoding conserved elements (CE) of the HIV-1 Gag core protein, p24Gag, as a therapeutic vaccine in HIV-1 infected persons who were on antiretroviral therapy (ART).” (3)

Let’s pause here. A “therapeutic vaccine” is not a preventive vaccine. As ScienceDirect explains, “Therapeutic vaccines are immunotherapies that treat existing diseases—such as cancer or chronic infections (e.g., HIV, HBV)—by training the patient’s immune system to attack diseased cells. Unlike preventative vaccines, these are administered after diagnosis to halt disease progression, reduce symptoms, or eliminate remaining cells.” (5)

Therefore, these patients were not given a “DNA vaccine”; they were given a treatment.

It was during this first step in the clinical trial that electroporation—the electric shock method of delivering medication—that made Perrault scream in response.

Second, study participants were later given a “Toll-like receptor (TLR) agonist,” which is a substance that binds to and activates TLRs, “specialized receptors on immune cells that detect pathogens. By mimicking bacteria or viruses, TLRs trigger the innate immune system, inducing inflammation to fight infections or cancer, and act as potent vaccine adjuvants.” (6)

Again: No HIV vaccine was used in this clinical trial.

Third, patients were given broadly neutralizing antibodies (bNAbs). According to a study published on ViiV Healthcare: “Broadly neutralizing antibodies (bNAbs) are
rare, potent antibodies that recognize and neutralize diverse strains of rapidly mutating viruses, most notably HIV-1, by targeting conserved, unchanging regions. Unlike conventional antibodies, they develop in some individuals after years of infection and are being developed for HIV prevention, long-acting treatment, and vaccine design.” (7)

Again: Broadly neutralizing antibodies are not a vaccine.

Finally, after eight months of clinical trial participation, patients were instructed to discontinue ART so the researchers could determine if “viral load” rebounded or stayed (presumably) suppressed by the study’s treatments. (2)

At the end of this proof-of-concept trial, what was the result?

“The protocol defined post-treatment control [of HIV] as maintaining a viral load ≤400 copies per ml at two-thirds of the timepoints for a period of ≥24 weeks,” these researchers explained. (2)

“Seven out of the ten participants exhibited post-intervention control after pausing ART, independent of residual bNAb plasma levels,” Deeks and colleagues reported. “Robust expansion of activated CD8+ T cells early in response to rebounding virus correlated with a lower median viral load after peak viraemia off ART. These data suggest that combination immunotherapy approaches might prove effective in inducing sustained control of HIV by slowing rebound and improving CD8+ T cell responses, and that these approaches should continue to be optimized.” (2)

Furthermore, they concluded: “To our knowledge, our study is the first to demonstrate that, after combination immunotherapy, individuals with a more robust in vivo CD8+ T cell response to emerging virus after pausing ART go on to establish better control of HIV.” (2)

But what if HIV is not the virus destroying these clinical trial participants’ immune systems? As with all NIH-backed trials, that question was not addressed.

And while electroporation is increasingly used in treating cancers, there surely must be technologies in the pipeline that are less painful and frightening.

Tom Perrault told SFGATE that “he took part in the study to make things even better for the next generation,” an admirable reason for sure. (1)

But could we perhaps find another method for forcing foreign chemicals into peoples’ cells—maybe one that doesn’t make study participants scream?

BIBLIOGRAPHY
1. Gillian Mohney. “After ‘unprecedented’ results, SF researchers get closer to HIV cure. ‘We haven’t quite made it to the promised land. We’re getting close.’ ” SFGATE, April 15, 2026. https://www.sfgate.com/bayarea/article/sf-hiv-cure-california-21244134.php
2. Peluso, M.J., Sandel, D.A., Deitchman, A.N. et al. “Correlates of HIV-1 control after combination immunotherapy.” Nature 650, 187–195 (2026). https://doi.org/10.1038/s41586-025-09929-5
3. “HIV-1-Gag Conserved-Element DNA Vaccine (p24CE) Study.” ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT03560258
4. “Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents With HIV.” HIV.gov. https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-arv/adverse-effects-antiretroviral-medications
5. “Therapeutic Vaccine.” ScienceDirect Topics. https://clinicaltrials.gov/study/NCT04357821
6. “Toll Like Receptor Agonist —an Overview,” ScienceDirect Topics. https://www.sciencedirect.com/topics/medicine-and-dentistry/toll-like-receptor-agonist#:~:text=Toll%2Dlike%20receptors%20(TLRs),some%20evidence%20of%20antitumor%20activity.
7. Jan Losos. “Broadly Neutralising Antibodies Are Being Explored for Potential HIV Treatment, Prevention, and Perhaps Even Cure or Long-Term Remission.” ViiV Healthcare. https://viivhealthcare.com/ending-hiv/stories/science-and-innovation/broadly-neutralising-antibodies/

Gilead Sciences abandons novel HIV drug trials after FDA refuses to lift ban

Gilead is certainly no stranger to criticism; the Truvada lawsuits, involving over 26,000 total plaintiffs, continue to move through the courts. These two trials did not involved a Truvada type drug. One was studying the tablet form of lenacapavir and the other was a novel drug meant to be taken weekly. Safety concerns surrounding lenacapavir should be concerning, since that medication is being pushed hard as a preventative. Will it meet the same fate as AZT?

Let’s dive in to the piece.

Major U.S. pharmaceutical giant Gilead Sciences has completely terminated the clinical study Wonders‑2, which was testing the company’s new HIV drugs. The decision was made after the U.S. Food and Drug Administration (FDA) refused to lift a previously imposed clinical hold on the trials, reported Fierce Biotech, citing representatives of the manufacturer and the agency.

What might have happened had the FDA lifted the clinical hold? Would Gilead have moved forward regardless? Previous actions indicate this is a strong possibility.

The Wonders‑2 study began as a Phase II/III trial and included 73 patients. In parallel, another, larger study, Wonders‑1, involving approximately 675 people, was underway. Both trials tested a combination of two experimental drugs – GS‑1720 and GS‑4182 – comparing it with existing treatment.

GS‑4182 is a tablet formulation of the already approved lenacapavir, which Gilead sells under the brand name Sunlenca. GS‑1720 is an experimental therapy designed for weekly dosing.

That first study is certainly underpowered, with only 73 participants, who were receiving a kind of combination therapy consisting of lenacapavir along with this novel drug. I thought lenacapavir was near perfect? Why then do we need to administer it in combination? It is also unclear whether these trials were for PrEP or for ARVs. I will yet again remind you that lenacapavir was originally developed to treat “heavily treatment resistant” “HIV” positive individuals and NOT as a preventative.

Both studies were suspended in June 2025 due to safety concerns. In some patients receiving the drug combination, levels of CD4+ cells (a key indicator of immune function in HIV patients) and total white blood cell counts dropped. Later, blood counts in participants of the small study returned to normal. Despite this, the FDA did not lift the hold. Consequently, the company decided not to continue Wonders‑2 and has now fully terminated that trial.

So the drug combination caused T cells to decrease—in other words, it induced AIDS in these patients, definitionally. It isn’t clear whether the safety concerns stemmed from one or both drugs in the combination; regardless, this should raise yet more red flags with lenacapavir.

Gilead Sciences is currently transitioning participants to standard care and continues developing other drugs, including long‑acting regimens based on lenacapavir – one of its key HIV medicines. Last year, the WHO included this drug in its recommendations for the treatment and prevention of HIV and sexually transmitted infections. It became the first FDA‑approved drug for pre‑exposure prophylaxis (PrEP) of HIV that requires administration only twice a year.

This conclusion is extremely confusing. So the lenacapavir drug, in combination, led to a decrease in both T cells and white blood cells more generally, yet we wrap up with what is effectively an ad for the drug that is under fire for its “safety.” I suppose this is par for the course in “HIV” medicine, as we are sadly aware. I fear that PrEP just generally is hastening an ever further loosening of standards regarding these drugs’ safety and efficacy. What could possibly go wrong pushing lenacapavir on the general population? This trial provides a hint of an answer to that question; this drug will not improve “in the wild.”

As always, let me know what you think in the comments.

Engelhart follows Tabitha’s efforts to understand her husband’s condition—called a “vegetative state” or VS—and improve his care. While the severe heart attack and a lack of the insulin Aaron needed but hadn’t taken had apparently triggered his collapse, he suffered severe brain injury from lack of oxygen before hospital personnel got his heart beating. Aaron’s brain swelled “so much that his brain pushed outward against his skull, partly flattening the folds and ridges that covered its surface,” Engelhart reported. (1)

“Tabitha remembers a doctor explaining that the human brain is composed of distinct regions, and that in Aaron’s case, it was ‘the part of the brain that makes you you’ that was damaged,” according to Engelhart. (1)

The most hopeful information Tabitha was given was that Aaron might recover enough to be in a state of “minimal consciousness.” The doctors weren’t terribly hopeful and gave Tabitha two alternatives: remove Aaron from the machines that were feeding and breathing for him or find a nursing home to care for him. (1)

So began Tabitha’s dive into the brain science that attempts to discover how well an injured brain can recover and function. The first hopeful information she found described some patients who had “cognitive motor dissociation (CMD),” a state in which the brain is dissociated from the body it can no longer control. However, in some cases, the brain still functions. (1)

Back in 2002, a research team from the JFK Johnson Rehabilitation Institute (Edison, NJ) began studying what they called the “minimally conscious state” or MCS. (2)

This group, led by neurologist N.D. Zasler, explained the condition and the reasons for understanding it better in their paper:

“There is a subgroup of patients with severe alteration in consciousness who do not meet diagnostic criteria for coma or the vegetative state (VS). These patients demonstrate inconsistent but discernible evidence of consciousness. It is important to distinguish patients in MCS from those in coma and VS because preliminary findings suggest that there are meaningful differences in outcome.” (2)

In other words: Patients who appear outwardly to be in a vegetative state or coma may in fact be in a minimally conscious state. It appears they can hear, respond to some high-level orders (“lift your finger” or “blink your eyes”), and their conditions are “distinguished from VS by the partial preservation of conscious awareness.” (2)

The objective of this 2002 paper was to define diagnostic criteria for the minimally conscious state, and they began by looking for published research that might indicate awareness of it. Members of the team performed a MEDLINE literature search for “published articles using the key words coma, vegetative state, minimally responsive state, stupor, slow-to-recover, severe disability, and Glasgow Coma Scale. These terms were then cross-indexed with brain injury, diagnosis, and outcome in eight different permutations to retrieve articles that included patients who did not meet diagnostic criteria for VS, but at the same time, were not considered fully conscious.” They found a total of 260 such articles, but only five noted patients who had “inconsistent signs of consciousness” and so were not in a permanent vegetative state. (2)

The definition of minimal consciousness they agreed upon for future research was: “The minimally conscious state is a condition of severely altered consciousness in which minimal but definite behavioral evidence of self or environmental awareness is demonstrated.” (2)

Two patient responses were suggested as being diagnostic of MCS:
1) functional interactive communication (being able to communicate via yes/no signals, writing, verbalization), and
2) functional use of two different objects (i.e., using them appropriately). (2)

These researchers concluded:

“MCS is characterized by inconsistent but clearly discernible behavioral evidence of consciousness and can be distinguished from coma and VS by documenting the presence of specific behavioral features not found in either of these conditions. Patients may evolve to MCS from coma or VS after acute brain injury. MCS may also result from degenerative or congenital nervous system disorders. This condition is often transient but may also exist as a permanent outcome. Defining MCS should promote further research on its epidemiology, neuropathology, natural history, and management.” (2)

Twenty-two years later—in 2024—these researchers (with others) published an international, multi-site, 353-patient study of “disorders of consciousness.” They studied “cognitive motor dissociation” (CMD), a condition in which a patient with a severe brain injury appears unresponsive but shows “clear evidence of conscious awareness” during advanced brain imaging and/or electrical monitoring. (3)

Functional MRIs (the brain imaging part) and EEGs (the electrical monitoring part) were used in this follow-up study.

You may already know that MRIs use magnetic signals to image the structure of the brain. A functional MRI—fMRI—is less like a photo of the brain and more like a video of what it’s doing in real time. When neurons fire in the brain, they use extra oxygen. Brain areas that have extra oxygen emit a different magnetic signal than do inactive, oxygen-poor areas. The active, oxygen-rich areas of the brain “light up” during a fMRI.

Electroencephalograms or EEGs, on the other hand, measure the electrical activity of neurons in the brain. Used together, these two technologies can map what areas of the brain are working at any point in time.

So how do fMRIs and EEGs help detect consciousness in a person unable to move or speak? It turns out that performing an action and thinking about performing this action cause the brain to light up in the very same area.

For the usual reasons in clinical trials, results from only 241 people who’d been diagnosed with coma or vegetative state were reported. These patients had undergone EEG, fMRI, or both. (3)

The study produced a surprising result: 60 of these patients—25%—”had a response to commands on task-based fMRI, task-based EEG, or both.” (3)

Fully one-quarter of patients previously judged to have none or almost no brain activity—because they’d been diagnosed with coma or vegetative state—were able to respond to instructions such as “imagine you’re playing tennis.” The correct area of their brains lit up as if they were, in fact, playing tennis. (3)

Previously, only 10-20% of people diagnosed with coma or vegetative state were found to have cognitive motor dissociation, in which their brains received verbal instructions and were able to imagine carrying out those instructions. (3)

This astonishing, enlightening, hopeful finding, however, currently has no application outside of clinical trials, as Tabitha discovered when trying to have her husband tested for cognitive activity. The technology is too expensive for most hospitals to own, and because most hospitals don’t own it, their staff isn’t trained to use it. (1)

It has, nevertheless, raised a plethora of ethical and moral questions.

If 25% of people thought to be in a vegetative state are actually aware of everything around them, it seems to me that we need to reassess the treatments—or lack of—provided them.

What about disconnecting life support to people like Aaron, Tabitha’s husband, whose body is being kept alive by machines but who might actually be able to hear and understand everything happening in his environment?

Who’s going to decide which patients with brain injuries become organ donors? On what basis? Will more testing be required to make sure such patients can’t hear discussions about themselves and their potential organ donations?

And all too often, politics, economics and religious beliefs in families (and the wider world) collide when caring for a brain-injured person. Can families be assured that their friend or relative is actually conscious, if unable to express it physically—or the reverse, that the brain injury indeed has no possible chance of healing?

How do we protect the helpless? Who decides? And how many more decades will it take to mount a good-faith effort to make sure no one who is conscious and (even minimally) able to communicate dies from uninformed treatment?

BIBLIOGRAPHY
1. Katie Engelhart. “Vegetative Patients May Be More Aware Than We Know.” New York Times Magazine, April 9, 2026. https://www.nytimes.com/2026/04/09/magazine/vegetative-states-conscious-aware.html?campaign_id=61&emc=edit_ts_20260409&instance_id=173823&nl=the-great-read&regi_id=1052086&segment_id=217980&user_id=61b722419e82a04fdcfca7c95617a5f2&login=email&auth=login-email
2. Joseph T Giacino, S Ashwal, N Childs, R Cranford, B Jennett, DI Katz, JP Kelly, JH Rosenberg, J Whyte, RD Zafonte, ND Zasler. “The Minimally Conscious State: Definition and Diagnostic Criteria.” Neurology. 2002 Feb 12;58(3):349-53. doi: 10.1212/wnl.58.3.349.
3. Yelena G. Bodien, Ph.D., Judith Allanson, F.R.C.P., Ph.D., Paolo Cardone, Arthur Bonhomme, M.D., Jerina Carmona, M.P.H., Camille Chatelle, Ph.D., Srivas Chennu, Ph.D., +31 [authors], and Nicholas D. Schiff, M.D. “Cognitive Motor Dissociation in Disorders of Consciousness.” August 14, 2024. VOL. 391 NO. 7. N Engl J Med 2024;391:598-60. DOI: 10.1056/NEJMoa2400645

Epstein email involving Harvard professor reveals cryptic 'spy' reference

Here are some details from the piece (emphasis mine):

A newly surfaced email exchange from the Jeffrey Epstein files shows an obscure message from Harvard University professor Martin Nowak to the late sex offender, prompting questions about the language used in the correspondence.

Nowak wrote the email, dated March 10, 2014, to Epstein that “our spy was captured after completing her mission.”

Epstein replied by asking, “Did you torture her,” according to the document released by the US Justice Department.

“Did you torture her?” What? This is extremely disturbing. And who is she, exactly? The piece is unclear on that, but read on.

While the exchange does not explain what the messages referred to, nor does it identify any individuals or events, the wording has drawn attention on social media following the release of the documents, with some users describing the exchange as “disturbing.”

Yes. Yes, this is disturbing. We know that Nowak has been placed on administrative leave due to his ties to Epstein, but this piece reveals a possibly much deeper level of enmeshment. The following excerpt discusses Nowak’s alleged travels with Epstein. Allegedly, he may have accompanied Epstein to St. Thomas Island, which is close to the famed “Epstein Island.”

Other emails involving Nowak also appeared in the files, indicating continued contact between the Harvard professor and Epstein for several years. Some correspondence referenced private meetings and social engagements involving prominent academics.

Another document revealed a discussion from February 2014 and included Nowak’s name with details about a planned trip.

The document showed that someone named Anna Yermakova would accompany Nowak, and also revealed information about their seating arrangements on the plane.

The travel details attached to the emails state that the pair would fly from Boston to St. Thomas Island, which is near the islands owned by Epstein in the US Virgin Islands, and return two days later.

This isn’t the only trip Nowak allegedly took or planned to take. Read on:

The emails also show that similar travel arrangements were made for Nowak in 2012, with Epstein personally involved in the correspondence.

In another email from February 2014, Epstein’s assistant Lesley Groff said, “Reminder Martin Nowak is asking if he can go to your island march 1.”

Nowak has not yet been accused of criminal wrongdoing. But Harvard University placed him on paid administrative leave in 2020 after conducting an internal review of its historical ties to Epstein.

Not yet. As a reminder, Nowak has recently been put on administrative leave for a second time.

That review found Epstein had access to Harvard facilities and sought to associate himself with the university following his 2008 conviction in the US state of Florida for soliciting sex from a minor.

Nowak continues to be a professor of mathematics and biology at Harvard University.

What the outcome of this administrative leave will be is unclear at this time, as is whether Nowak will receive further consequences for his relationship with Epstein. Certainly, if he has been involved with some of the more salacious aspects of Epstein’s inner circle, he ought to be called to answer.

Again, this is a developing story, so stay tuned for more details. The takeaway for me from this is that corruption in one’s personal life tends to bleed into the professional, and vice versa.

Per The Harvard Crimson (emphasis mine):

Nowak was among the Harvard affiliates most closely connected to Epstein. He corresponded frequently with the financier and played a central role in integrating him into Harvard’s academic circles — arranging visits, introducing him to faculty, and cultivating relationships on his behalf.

Epstein also funded Nowak’s Program for Evolutionary Development and helped secure an office space in Harvard Square, where he regularly met with Harvard professors.

Even his Wikipedia page is full of Epstein allegations, including the jaw dropping reporting that Epstein left him $5 million in trust:

Nowak maintained a close personal and financial relationship with the financier and convicted sex offender Jeffrey Epstein.^[33] The preface of his 2011 textbook, Evolutionary Dynamics: Exploring the Equations of Life, ends with “I thank Jeffrey Epstein for many ideas and for letting me participate in his passionate pursuit of knowledge in all its forms.”^[34]

In response to the revelations of Epstein’s support of Nowak and his lab (the Program for Evolutionary Dynamics), in 2021 Nowak was suspended from supervising undergraduate research for two years, and the institute was permanently closed.^[35][36] Harvard’s review, leading to the suspension, uncovered that Epstein had maintained access to a personal office in Nowak’s lab for 9 years, even after his conviction for sex crimes, and used the office over 40 times, “typically accompanied by young women serving as his assistants”.^[37]

Epstein used his office.

In 2023, Harvard lifted the sanctions against Nowak, and he remains on the faculty, jointly appointed in the Department of Mathematics and the Department of Organismic and Evolutionary Biology.^[38]

On February 25, 2026, Harvard announced that Nowak had been placed on administrative leave from the university after a formal investigation was opened by the Faculty of Arts and Sciences.^[39]

Epstein left Nowak US$5,000,000 in his trust.^[40]

The resignation from the Austrian Academy was only reported two days ago, so it’s safe to say this story is unfolding. Dr. Nowak is very familiar to me, since the models I studied in my doctoral work were inspired by his very elegant models that he published together with Dr. George Shaw, the very Shaw who was involved in the famous 1996 papers by Ho and colleagues that we have discussed multiple times. It is safe to say that, alongside Alan Perelson of Los Alamos, Nowak is one of the most well known modelers of “HIV” immune dynamics. This story is a huge scandal, and it will only get worse for Nowak, I imagine.

Stay tuned for developments.

Hi and welcome to Denialism and Other Oddities. This Substack replaces my old blog with the same name. I created that blog back in 2009 as a companion to my book Denying AIDS: Pseudoscience, Conspiracy Theories, and Human Tragedy. Like all books, Denying AIDS was frozen in time, all while AIDS denialism marched on. I created the blog to post updates as AIDS denialists spewed out their nutty ideas and spread deadly falsehoods. At times denialists commented on my blog, which was always interesting. The blog also provided an opportunity for feedback from readers.

Right off the bat, take note of his inflammatory, decidedly non-collegial tone. He’s so unprofessional. “AIDS denialists” have ideas that are “nutty” and potentially murderous. We’re not just asking questions and demanding accountability, we’re lunatics.

As the years went by, the relevance of AIDS denialism seemed to fade. Their leading voice, Christine Maggiore, had died of AIDS. Their greatest achievement, the denialism of South African President Thabo Mbeki, came to an end. And HIV treatments became so effective they squelched out even the loudest deniers.

Christine Maggiore’s story is far more nuanced than to simply say she “died of AIDS.” Christine was healthy until just days before her death; she did not exhibit any signs of “progression to AIDS” or “HIV disease.” Her decline was far too swift to attribute to “HIV.” However, the HIV orthodoxists have a permanent gift in that everyone dies. It’s the ultimate “gotcha,” and it is practically impossible to refute. Perhaps, all told, we all die of AIDS eventually. This is certainly true of CFS and other non-HIV cases of AIDS.

I’ll discuss the wonderful “treatments” below. As a teaser, check out what has happened with the protease inhibitors —they have completely stopped being prescribed because of the metabolic toxicities, yet they are credited with ending AIDS, which is ridiculous. We’re now back to prescribing Truvada, which is effectively AZT 2.0. Descovy is no better. Both drugs are being given to “HIV” negative people as PrEP. Let that sink in.

Furthermore, recall that there are currently multiple lawsuits, including a class action lawsuit involving 26,000 plaintiffs, brought against Gilead Sciences for covering up Truvada’s known causation of kidney damage, bone loss, and more. It even made the New York Times, albeit the business section.

And then came COVID-19.

Just like that, AIDS denialists were back. They joined the COVID denial bandwagon. They offered COVID deniers a playbook. They added to the anti-vaccine insanity. They created chaos through misinformation, like saying there is no proof that COVID is caused by a virus, but rather by 5G networks. They cast doubt on efforts to mitigate the spread of COVID. They pointed out how Anthony Fauci had lied about HIV causing AIDS, and he was at it again with COVID. They created conspiracy theories to offer proof for their wacky ideas. They had a new and much bigger audience across social media platforms, like Substack.

AIDS deniers had their dreams come true in Robert F. Kennedy, Jr., the most dangerous AIDS denialist since Thabo Mbeki.

Does he not know that RFKJ specifically said he takes no position on whether “HIV” causes AIDS? How can he possibly be the most dangerous if he hasn’t even committed to a position?

It was suggested to me that Denying AIDS needed an update. I agreed. So, I undertook a second edition. As the craziness got crazier, the second edition started to look a lot more like a whole new book. That is why the title is different – Denying AIDS: Pseudoscience and Conspiracy Theories in a Post-COVID World. And as the release of Denying AIDS-2 (as I call it) nears, it seems that a new ‘blog’ is in order.

Oh God, he’s rereleasing his book too. I guess both sides can play this game.

And here we are.

I will be posting as denialism continues to evolve. Unfortunately, that seems like it will be a while. I am monitoring relevant events daily. I follow the AIDS deniers and their antics. I am also watching the undoing of the U.S. public health system. RFK, Jr. does crazy every day, and we need to pay attention.

Here again we see the completely unprofessional language again—AIDS questioners (not deniers) don’t ask relevant questions; their observations are merely “antics,” and RFKJ “does crazy?”

I track the dismantling of global health programs by Marco Rubio and the rise of pseudoscience at the NIH and CDC. I am paying attention to the growing anti-vaccine movement and increases in vaccine-preventable disease outbreaks. I follow the quacks, cranks, and other oddities of relevance to public health. When I see something, I will post it.

Buckle up. It’s going to be a wild ride.

Well, he’s is certainly mudslinging and acting in an overall not very collegial way.

Let’s go back to the first bolded statement—notice he assumes the wrongness of “denialists” without any proof at all. And the manner in which he discusses AIDS critics is nothing less than bullying behavior.

“And HIV treatments became so effective they squelched out even the loudest deniers,” he says. Tell that to the 26,000+ victims of Truvada. There are entire Reddit threads on this topic. Recall also that the mechanism of action of Truvada; it is a NRTI drug and as such terminates DNA synthesis in the same manner as does AZT. Furthermore, we are now giving these drugs to patients with no hint of “HIV” as PrEP. I can’t see how that could possibly go wrong. Oh, wait.

I will end this post with the following offer:

Dr. Kalichman, I will be happy to debate you anytime, on substack live or elsewhere. Take that to the bank.

Appendix:

Perplexity AI, to conclude, sums up his unprofessional tone with the following twenty questions:

1. Is it professional and ethical for a psychologist to call someone crazy who reports on the 26,000 victims of Truvada who are suing the manufacturer for the damage done to them?

2. Is it professional and ethical for a psychologist to call someone crazy for questioning whether the original identification of HIV as the sole cause of AIDS in the 1980s may have been a scientific mistake?

3. Is it professional and ethical for a psychologist to call someone crazy for pointing out that patients were not fully informed about the risks and limitations of HIV tests and antiretroviral drugs?

4. Is it professional and ethical for a psychologist to call someone crazy for arguing that the history of AIDS medicine and activism has an underbelly of suppressed dissent and censored debate?

5. Is it professional and ethical for a psychologist to call someone crazy for asking whether expanding AIDS definitions in the 1990s helped make antiretroviral drugs look more effective than they really were?

6. Is it professional and ethical for a psychologist to call someone crazy for questioning whether AIDS surveillance statistics in Africa may have been distorted by weak data and political agendas?

7. Is it professional and ethical for a psychologist to call someone crazy for suggesting that non‑HIV infections like cytomegalovirus and other herpesviruses may have played a larger role in AIDS cases than officially acknowledged?

8. Is it professional and ethical for a psychologist to call someone crazy for doubting that mass HIV testing campaigns, using imperfect tests, were an ethically sound public health strategy?

9. Is it professional and ethical for a psychologist to call someone crazy for highlighting that antiretroviral medications can themselves cause serious harm, including kidney and bone damage?

10. Is it professional and ethical for a psychologist to call someone crazy for arguing that billions in AIDS funding may have created perverse incentives to preserve a particular HIV‑centered narrative?

11. Is it professional and ethical for a psychologist to call someone crazy for asking whether the label “AIDS denialist” is being used to silence legitimate scientific criticism rather than to protect patients?

12. Is it professional and ethical for a psychologist to call someone crazy for criticizing the way AIDS activists have sometimes worked to suppress books and voices that challenge HIV orthodoxy?

13. Is it professional and ethical for a psychologist to call someone crazy for questioning whether long‑term toxicities of HIV drugs were minimized while safer alternatives were delayed?

14. Is it professional and ethical for a psychologist to call someone crazy for arguing that fear‑based AIDS messaging has traumatized generations without delivering proportionate benefits?

15. Is it professional and ethical for a psychologist to call someone crazy for suggesting that AIDS categories and case definitions were sometimes manipulated to support predetermined conclusions?

16. Is it professional and ethical for a psychologist to call someone crazy for drawing attention to tragic stories of people who trusted the AIDS establishment and later felt betrayed by the medical system?

17. Is it professional and ethical for a psychologist to call someone crazy for questioning whether the balance between drug company profits and patient safety was ever honestly confronted in AIDS policy?

18. Is it professional and ethical for a psychologist to call someone crazy for arguing that genuine informed consent in AIDS treatment requires honest discussion of test uncertainties and drug risks?

19. Is it professional and ethical for a psychologist to call someone crazy for noting that critics of HIV‑centered AIDS models have sometimes been personally vilified instead of substantively answered?

20. Is it professional and ethical for a psychologist to call someone crazy for asking whether the AIDS narrative, as institutionalized, still serves patients’ best interests or mainly protects entrenched reputations and financial structures?

30M - I have been on Truvada for 11 years. Never had any issues until this year my urine became really yellow even when I drank a lot of water.

After some testing my eGFR has fluctuated between 56 and 58 for more than 3 months. My cyastin C came back okay, however my doctor diagnosed me with CKD.

He looked into medical literature on all my medications and believes my CKD was caused by Truvada. I wish I had known long ago how risky it could be on the kidneys. My previous doctor mentioned it but started having me test every 6 months instead of every 3 months since for years my kidney panels came back fine.

Since my diagnosis, my new doctor switched me to Descovy but noted that it also has a slight risk of kidney decline - much lower than Truvada though.

I just wanted to share my experience and give other patients something to consider or ask their doctors about. My doctor thinks that my kidneys may improve after a few months off of Truvada but I need to be tested every 3 months to see how things are going. I wish I had switched to Descovy in 2023 when my kidneys were still fine.

Here we have a real person (presumably) that has been undeniably harmed by Truvada. Is this person involved in any lawsuit? We know for sure that Truvada has been implicated in many cases of kidney disease.

There aren’t a lot of comments on this, but those that are don’t love Truvada. For example, “Gilead came up with Descovy to prevent all the toxicity of Truvada , I don't understand why people still use Truvada to this day.” How long will it be before the documented metabolic side effects of Descovy (aka “good Truvada”) become too frequent to ignore?

Also, just to remind you of tomorrow’s livestream at 4pm CDT. The working title is Fauci’s Self-Censorship. Hope to see many of you there!

You’ll get an email and a push notification when I go live. It’s been awhile and I’m looking forward to it.

AZT was the first effective treatment for HIV

Until it came along HIV/AIDS was a death sentence

AZT saved many lives and became an essential part of HIV treatment until it was replaced by better therapies

RFK Jr is talking nonsense here

Not great for a Health Secretary..

Nonsense? Why then is AZT barely used any longer? The most popular ARVs are tenofovir-based and don’t use AZT (zidovudine) at all. And as to ddI, I quote myself: “So in the trial, the death rate was 0.3% of the raw total, whereas “in the wild,” ddI performed more than ten times worse than it did in trials, at almost 4%.” If you want more information on AZT, recall John Lauritsen’s work from the 1980s and 1990s. Suffice it to say there is a reason we don’t prescribe it nowadays; and might I remind you that the new drugs aren’t so great either—from kidney failure to broken bones, Truvada itself has its own laundry list of problems.

Let’s check out some of the comments, shall we?

From user Sandy Glass: “Stop, with your revision of history. AZT killed those poor people.”

The top comment, from user edward j belanger (no caps) says: “It must pay off to be a gaslighting grifter because your posts continue to show up.”

And from user Karen Hoy: “AZT a wonder drug now? What else? Let’s put back lead on paint?”

The comments aren’t all critical of AZT though— there are some lunatics actually twisting themselves into mental knots defending it, like user Carrie Mae Garber: “I was at Int’l AIDS conference in 1996 … and there was soooo much hope with the studies showing the effectiveness of HAART - triple drug therapy.

And it all started with AZT.
My best friend and 1st boyfriend died in 1993 from AIDS.
RFK Jr can pack sand.”

This comment doesn’t say what Ms. Garber thinks it is saying. So because the triple drug therapies were so lauded, and so much more effective than AZT (though far from perfect, as the passage of time revealed—protease inhibitors are barely prescribed any longer), this is somehow evidence that AZT was amazing? Because it was first? This comment is so illogical it makes my head hurt.

Just a couple more:

From user Jojo: “This bull[shit] alone is a perfect example of why @RobertKennedyJr@SecKennedy should never be anywhere near the @NIH. A disgraced environmental lawyer peddling conspiracy theories is par for the course with this administration.”

Note what the comment doesn’t provide—any evidence at all that AZT was great. It’s just an ad hominem attack against RFKJ. There aren’t too many more comments defending AZT, so I’ll close with the following:

From user Nancy Collins: “Literally everything you say is false, propaganda masquerading as science. AZT was poison and killed thousands of people. It did not help HIV/AIDS patients whatsoever. Watch the movie Dallas Buyers Club.”

And finally, from user Quentin Farquar, addressing the OP: “Not only are you 100% wrong here, I'm pretty sure you know that you are 100% wrong.”

Does he though? Dr. Stone strikes me as a true believer. What do you think? Was AZT great, or even not totally bad?

I've never had a problem remembering to take my PrEP but was intrigued by not having to take an additional pill everyday so I decided to give Yeztugo a try. I read up on how it was injected and how big the needle was and everything and most of the stuff I read made it seem mild so I figured why not. I got my injections on Monday, March 2 and these photos are from March 6. The areas are still very red on my stomach and not as sore as they were a few days ago but still kinda sore. I'm not loving the big lump or sack under my skin, honestly I'm kind of self conscious about it. I'm hoping all of this will go down soon, but in 6 months I'll be moving back to Descovy for sure! "

You can click the link in the introductory paragraph to see the post, including pictures, and read the comments, some of which are crazy. My point in mentioning this here is that the AIDS establishment is placing all their hopes on lenacapavir to end the HIV AIDS epidemic. Clearly—as predicted—the side effects will prove too difficult for the number of people they want to take it to actually take it. At least they get the money from the initial injection.