I've had an allogenic stem cell transplant. It was hell. I no longer have cancer, so it was worth it. But HIV/AIDS (with standard treatment and testing) no longer significantly reduces life expectancy.
I have a hard time imagining a future where allogenic stem cell transplants are used to treat HIV. The procedures are incredibly risky and carry long term consequences (and in many cases, like mine, also unbearably painful for weeks).
To me, the most likely practical consequence of these findings is to spur on interest in using CRISPR (or other in-vivo genetic modification strategies) to alter the genome of an HIV patient to be "immune" to HIV. (A similar idea is used in treatment of some blood cancers. Chase the rabbit-hole of "CAR T Cell therapy" to get started.)
This explanation for the technique’s general inapplicability is touched on in the article.
It sounds like all of the HIV-cured were people that had a blood cancer that was, presumably, not responding to chemo, and for which they needed to get a new blood-making system grafted in. And, since this extremely risky procedure was a sunk cost, they rolled in the stem cell donor having an HIV resistant mutation as a might-as-well-since-we’re-in-there freebie while treating the blood cancer with a last ditch effort.
Inducing the HIV resistant mutation by other means is clearly the general way to go.
Finding an optimal donor match (via HLA typing) rarely returns many "perfect" matches. Perhaps there are systems that record both the CCR5 mutation and HLA typing, but I'd expect most donor matches, found via registries like https://bethematch.org/, will not have that information available.
I haven't dug into the weeds here (and, for personal emotional reasons, I will not), but I find it hard to believe the medical staffs would have seriously considered "can we find a donor that matches AND will possibly cure the HIV". The diagnosis-to-death timeline for many blood cancers is fast when other treatments don't work. Delaying a transplant by 2 weeks in order to find a slightly more optimal donor seems crazy. (Though I suppose the after-transplant care for someone with HIV might be trickier than those without HIV. But patients will be immune-compromised for at least months post-transplant, so maybe HIV isn't that big of a deal.)
HIV, in rich countries at least, is a managed condition these days. I'd imagine the only issues would be any sort of interactions between the don't-get-AIDS cocktail and the cancer drugs.
Perhaps the matching system has more data in Germany, or perhaps they really are just writing up happy accidents in which they discover that the patient lucked into a CCR5 donor and also already had low enough levels of HIV that the operation made a difference.
> I find it hard to believe the medical staffs would have seriously considered "can we find a donor that matches AND will possibly cure the HIV".
According to a report of the Tagesschau (belonging to the German public television chanel ARD),[1] the patient had leukemia and the doctors were looking for a fitting donor who was also missing a so-called CCR5 co-receptor. According to the report, people having such a gene mutation can be found especially in Central and Northern Europe.
The patient had already been treated in 2018, but is only now considered cured because he has not experienced any HIV symptoms since then.
I do not know whether it was relevant in this case, but Germany has a Central Bone Marrow Donor Registry with currently almost 10 million people registered.[2]
Indeed the article does not mention anything about the donors being chosen with HIV resistance in mind. So there is a good chance of this being a welcome side effect to the cancer treatment but not intentional.
"Last chance" describes both the way it was introduced to me by my medical team, and the circumstances around my SCT. I don't know how factually accurate it is, but my medical team had said there's about a 30% mortality rate caused by the SCT within about 90 days. (And, prior to chemotherapy ceasing to work, I'd been repeatedly reassured by medical staff with "chemo sucks but it isn't gonna kill you like a stem cell transplant would!")
Not endorsing the credibility of this article, but if you think this is interesting, you'll likely think https://www.variantbio.com is awesome.
They scour the globe looking for people groups, families, regions, etc. that have extremely rare immunities and other outlier characteristics in order to sequence their DNA.
> The stem cell transplantation is a complicated procedure that comes with many risks, and it is too risky to offer it as a cure for everyone with HIV.
Maybe it's just me but I hate when people/articles generalize like this. What are the risks? What are the benefits? What is the SPECIFIC hazard to health that is occurring? They just stick to general statements, because, in my opinion, they don't want to do the research. Either way the news itself is good to hear.
Stem cell transplantation is usually performed by bone marrow transplant, which is a pretty risky procedure: it involves destroying the recipient's own bone marrow to introduce the donor bone marrow, which can leave the recipient without significant numbers of white blood cells for a while, making them extremely vulnerable to infection.
In contrast, HAART for HIV is far less risky and far more safe, allowing people with HIV to live basically a normal life as long as their viral loads stay at undetectable limits.
That's the received wisdom, but it really seems trite.
HAART leaves people extremely vulnerable to infection as well, after all. The difference is that HAART means that point will come at some unpredictable point in the future, whereas a bone marrow transplant makes the window more predictable. And beyond that, it fails to consider the risks of decades of really toxic medication.
Is a bone marrow transplant really worse than decades of liver damage followed by developing AIDS eventually anyway?
Maybe, maybe not, but dismissing the heavy questions of a persons life with "basically normal" is not helpful.
> HAART leaves people extremely vulnerable to infection as well, after all. The difference is that HAART means that point will come at some unpredictable point in the future,
> And beyond that, it fails to consider the risks of decades of really toxic medication. Is a bone marrow transplant really worse than decades of liver damage followed by developing AIDS eventually anyway?
This is an outdated and objectively incorrect description of HAART.
> but dismissing the heavy questions of a persons life with "basically normal" is not helpful.
"Basically normal" is an approximately correct description of the life of most HIV+ people who have easy access to HAART. What's not helpful is responding to that with fearmongering based on incorrect and/or grossly outdated information.
Liver damage is a known adverse effect of both emtricitabine and tenofovir, which are extremely common antiretrovirals, an indisputable fact verifiable by anyone on the Internet.
There's a difference between fearmongering and informed consent, and I would ask you to refrain both from spreading misinformation and from making personal attacks. Accusing someone of "fearmongering" for pointing out risks you falsely say do not exist is inappropriate.
> Liver damage is a known adverse effect of both emtricitabine and tenofovir, which are extremely common antiretrovirals, an indisputable fact verifiable by anyone on the Internet.
Your comment literally claims that long-term HAART carries a significant (or even certain) risk of long-term liver damage, a claim which is baseless and unsupported.
You're also conflating acute adverse reactions - which are astronomically rare - with long-term side-effects, when there's no relationship between the two.
Not only are tenofovir and emtricitabine safe for the liver, but they are literally commonly prescribed for people who have chronic liver problems because they are so well tolerated. People who can't take Tylenol are able to take them. It's a gross mischaracterization to suggest that they cause "decades of liver damage", a claim which is soundly contradicted by medical literature.
> There's a difference between fearmongering and informed consent, and I would ask you to refrain both from spreading misinformation and from making personal attacks.
I never made any personal attack at any point.
I would, however, flip this request back at you and ask you to stop spreading misinformation, which is what you are clearly doing.
> Your insistence on gaslighting does not lend credibility to your other claims.
Your comparison to Tylenol is misleading. People aren't required to receive regular liver enzyme tests before being allowed to use Tylenol.
Read the guidelines yourself. Accusing people of fearmongering is a personal attack. If you think I'm wrong (and the FDA is wrong) about the risk of liver damage, feel free to present that evidence here (or better yet, to the FDA, so people can have better access to PrEP). Don't make false and ad hominem claims about my motivations.
> Your comparison to Tylenol is misleading. People aren't required to receive regular liver enzyme tests before being allowed to use Tylenol.
People aren't required to receive "regular liver enzyme tests" before taking these drugs either.
> free to present that evidence here
You've made a lot of claims without presenting any evidence to back any of them up. Moreover, your claims could be trivially debunked by even a cursory search. The burden is not on me or others to do that work when you yourself present zero evidence for any of the fantastical claims you make.
> Don't make false and ad hominem claims about my motivations.
I never made any claim about your motivation. "Fearmongering" is a specific, descriptive term about your actions, the effect they have on others, and their factual basis (or lack thereof).
On the other hand, you accused me of gaslighting (before editing it out of your comment and replacing it with a different accusation). That is an ad hominem attack, ascribing specific and malicious motivations.
I can't make claims about your country's medical system. In the U.S., where I am, regular liver enzyme tests are a requirement for a Truvada prescription. [EDIT: This is incorrect; I was mistaken.]
> In the U.S., where I am, regular liver enzyme tests are a requirement for a Truvada prescription.
Incorrect. A one-time test of liver function was previously sometimes suggested before starting PrEP specifically... but not for the reason you think. And it was never required.
Ongoing liver enzyme tests are neither required nor recommended. In fact, Truvada and Descovy were shown to be so safe during clinical trials that routine liver function tests are explicitly contraindicated for patients with no other comorbidities.
From 2011 to 2016, overall life expectancy at 21 years of age for individuals with HIV infection who initiated ART at a CD4 cell count of 500/μL or greater was 57.4 years (95% CI, 55.7-59.1 years) and for uninfected adults was 64.2 years (95% CI, 64.0-64.4 years), corresponding to a difference of 6.8 years (95% CI, 5.0-8.5 years)
The risk profile for a full bone marrow transplant for treating HIV vs HAART for a difference of ~5-9 years is just not there.
Based on their 2010 alloHCT volume, centers were categorized as low-volume (≤40 alloHCTs; N=42 centers, 1,900 recipients) or high-volume (>40 alloHCTs; N=41 centers, 9,637 recipients). 100-day survival was 86% (95% CI, 85–87%) in high-volume compared to 83% (95% CI, 81–85%) in low-volume centers (difference 3%; P<0.001). One-year survival was 62% (95% CI, 61–63%) and 56% (95% CI, 54–58%), respectively (difference 6%; P < 0.001).
You are literally getting a coin flip of surviving past 2 years after an allogeneic hematopoietic stem cell transplant. If I was given the choice of HAART and living a mostly normal lifespan, or maybe die with a coin flip chance in 2 years, I would pick HAART, no contest.
> You are literally getting a coin flip of surviving past 2 years after an allogeneic hematopoietic stem cell transplant. If I was given the choice of HAART and living a mostly normal lifespan, or maybe die with a coin flip chance in 2 years, I would pick HAART, no contest.
Not to mention that the "64 years" comparison is not the correct reference point here, because it's talking about people who were never infected with HIV in the first place, not people who have received a stem cell transplant.
The stem cell transplant almost certainly reduces both your lifespan and QALS in the long term, not just the first two years. Yes, it might be worth it if you have cancer, but it's not like it suddenly makes you clinically equivalent to a person who has never had HIV!
The article also does not mention the type of transplant: autologous or allogeneic.
As a recipient of an auto-transplant as part of cancer treatment, I perhaps can speak to the complexity of the procedure and the risks. For certain types of lymphomas, the best chance for life-long remission is through a stem-cell transplant.
- The patient first undergoes conventional chemotherapy to attempt to achieve remission.
- The patient then performs a barrage of tests to ensure that they are healthy enough to withstand the transplant procedure.
- The patient has a Hickman catheter installed. The catheter is a device with tube into the superior vena cava (one of the main return veins into the heart) and two external ports for drawing and returning blood and administering fluids and drugs.
- The patient performs mobilization and collection. During mobilization, the patient self-injects a growth factor drug that causes the body to produce extra hematopoietic stem cells and release them into the blood stream. During collection, the patient is connected to a centrifuge machine and the stem cells are collected and preserved.
- The patient enters the hospital for the transplant procedure. High dose chemotherapy is administered. For cancer treatment, the purpose of the chemotherapy is to destroy any cancer cells remaining in the body. Even though the patient may be in remission from first-line chemo, some cancers can return from just a few remaining cancer cells. A side-effect of the high-dose chemotherapy is the destruction of the body's ability to produce blood.
- After chemotherapy, the patient's own stem cells are injected. Within 7 to 10 days, these cells will recolonize the bone marrow, "engraft" and begin producing blood.
- Once the patient's blood cell counts are on the rise and the patient is otherwise stable, he is sent home. The patient typically needs live-in care at home for about 30 days (the patient's blood counts are still very low and a normally trivial injury from cooking or cleaning could be deadly).
The risks of the procedure are from the high-dose chemotherapy and the fragile state of the immune system after the transplant. After a transplant, _all_ immune memory is erased and the patient is as a newborn as far as immune system capability is concerned.
The risks include:
- Chemo related organ damage to heart, lungs, kidneys and liver.
- Chemo-induced pneumonitis.
- Graft failure (e.g. failure of the stem cells to recolonize the bone marrow).
- Infection (since the immune system is destroyed during the process, a normally minor infection can be deadly).
According to my transplant doctor, the auto-transplant process has about a 2% risk of death.
The benefits are that the probability of a cancer relapse is significantly reduced (say 90% risk to 50% risk).
For the patient, the process is very difficult and recovery time is approximately one year.
All four of these patients had undergone stem cell transplants for their blood cancer treatment. Their donors also had the same HIV-resistant mutation that deletes a protein called CCR5, which HIV normally uses to enter the cell. Only 1% of the total population carries this genetic mutation that makes them resistant to HIV.
The article is horribly wrong about CCR5 being the only pathway of the HI Virus to infect your cells and ultimately cause AIDS.
A problem of this approach is that, while CCR5 is the major co-receptor by which HIV infects cells, it is not the only such co-receptor. It is possible that under selective pressure HIV will evolve to use another co-receptor. [1]
Why this treatment still worked is because:
However, examination of viral resistance to AD101, molecular antagonist of CCR5, indicated that resistant viruses did not switch to another co-receptor (CXCR4), but persisted in using CCR5: they either bound to alternative domains of CCR5 or to the receptor at a higher affinity. However, because there is still another co-receptor available, it is probable that lacking the CCR5 gene does not make one immune to the virus; it would simply be more challenging for the individual to contract it. [1]
So a mixture of anti-retroviral treatments, which suppress the HIV replication to a point of not showing up in PCR tests anymore (while taking the medication), and (partially?) inhibiting the remaining viruses from infecting cells via the CCR5 pathway, further limiting their replication, caused these patients to be cured.
I don't know if the replication slowed down so much that their body was able to kick HIV out once and for all, or blocked it outright because the already reduced number of viruses simply could not beat the odds of infecting via a alternative pathway. Kudos to the researchers!
Why is this important: The CRISPR babies[2] had this exact gene removed, and everybody claimed that he cured them from ever getting HIV, even though it's simply not true.
Note that there are also drugs which disable CCR5, without gene modification (Selzentry).
It's been a few years now but I used to work on research on this particular alternative receptor.
To handwave and simplify a bit CCR5 is the dominant pathway for the virus to spread in a healthy patient. HIV tends to mutate in patients from attaching to CCR5 (called phenotype R5) to CXCR4 (called X4) once the immune system is weaker. Patients with the X4 are not as infectious as a healthy immune system can fend it off.
So CCR5 is more or less the only pathway for the virus to infect a healthy host, as far as I can remember.
Your quoted line from the article stated: "Their donors also had the same HIV-resistant mutation that deletes a protein called CCR5, which HIV normally uses to enter the cell. Only 1% of the total population carries this genetic mutation that makes them resistant to HIV."
Then you stated: "The article is horribly wrong about CCR5 being the only pathway of the HI Virus to infect your cells and ultimately cause AIDS."
I'm not quite sure how you made the leap from "... which HIV normally uses to enter the cell" to thinking the article stated "... CCR5 being the only pathway of the HI Virus to infect your cells", but :shrug:
Your right, horribly is probably the wrong word, but the same quote said [..] this genetic mutation that makes them resistant to HIV.
I don't care so much about the wording in this article, but there have been a lot of efforts for HIV "cures" in the direction of disable CCR5 = disable HIV, which unfortunately is not true.
Also when you disable CCR5 on more and more people, the selective pressure may evolve to HIV which primarily targets CXCR4.
The way seems to anti-retroviral drugs, and then finish it with CCR5 inhibition.
>The article is horribly wrong about CCR5 being the only pathway of the HI Virus to infect your cells and ultimately cause AIDS.
I think the article was just simplifying a very difficult topic in order to reach a mass audience. Very enlightening information that you've added to more illuminate the topic, so chapeau.
> Only 1% of the total population carries this genetic mutation that makes them resistant to HIV.
Wow, I didn't even know that you can be immune to HIV. It's only a matter of time before we have technologies to change our genetic code or at least the genetic code of two cells before they form an embryo.
> It's only a matter of time before we have technologies to change our genetic code or at least the genetic code of two cells before they form an embryo.
> Wow, I didn't even know that you can be immune to HIV.
HIV contains some code which use to convert a cell to be a zombie (afaik that cell's vulnerable place in cell's DNA is called CD4). But some people has that part of cell's DNA slightly different, not better not worse but different, therefore not vulnerable to that special code. The HIV for different cells is yet to be discovered.
When we will have understanding of how to change the DNA code (implementing is really easy tbh), than any malintentioned person might develop new viruses shaping some known ones to be even more destructive.
Recently there was a post on HN about some child whose genetic disease was cured by inserting DNA (can't remember the specifics). I wonder if something similar could be done with HIV. Obviously you'd have to insert a mutation for the CCR5 protein. Then the problem is you have all this bone marrow that's still producing white blood cells of the old type, so you'd need some way of killing off the old bone marrow cells without the right mutation and replacing them with the new ones.
Nice, but I wonder how long before it's going to be an option for all those who want it (even ignoring whether managing HIV may be better then curing it).
I'm still waiting for ocumetics bionic lenses to end glasses and contact lenses (ha ha ha, they're probably still collecting money from all the parties they should be destroying) and I lost hope we'll ever see RISUG, the male permanent but removable contraceptive without cancer-causing hormones.
Michael Levin is doing that. He's researching morphogenesis, but he also found that cancer is related to that. Basically, all cells communicate with each other with electric potentials to work towards a common goal, like forming an organ or a limb. Cancer happens when that communication is disrupted. It disappears when it's restored.
Stem cell transplantation is probably not the most effective way to end HIV due to its severe risks and cost: it's much more likely preventative measures like PrEP/PEP and treatments like HAART are much more viable long-term solutions.
Seems to me like every improvement in medical science will be accompanied by a corresponding decrease in individual responsibility. Just like hardware and software.
I've heard young people basically say 'HIV isn't a big deal nowadays so no need to worry'.
But you suddenly become dependent on someone else, in this case what if they suddenly increase the price of the HIV medication? Or there is a global shortage? Or we discover that a subpopulation has a resistant variant?
I guess it's just different opinions. What I'm saying is that when given the opportunity to get rid of fear, we should. Same way I'm not afraid of wildlife attacking me, or cholera.
I probably won't die if I get food poisoning but I'm not going to go around eating raw meat for the thrill of it and expect the taxpayer to pay for me every time I get sick.
Ah, so underlying the 'moral' argument is the uncontrollable FEAR that you, a wealthy but unadventurous person, are somehow subsidizing other less wealthy people as they enjoy their lives.
No I am saying young people have gotten the impression that it's completely cured now and can be as reckless as they want which sounds to be incorrect according to the other comments here.
Do you visit gay sex clubs? I do, and I would say that it is far from true that people feel they can be as reckless as they want. Rather, they are generally risk-aware, but within a context where the risk tradeoffs are completely different to the AIDS awareness climate of the late 80s and 90s.
For example, there is a distinction between low risk activity such as oral sex and higher risk activity such as anal. The latter will often involve a brief discussion of risk: condom use, PrEP, status, so that both participants are on the same page.
If HIV were really not a big deal anymore, why should people still worry? If you could have risk-free sex with the seediest of characters, why would it be "not a responsible thing" to do so?
It's definitely not - which is why I said "if it really were". Hopefully, one day technology will get it there.
Note that the treatment in this article, as others have pointed out, is really not that. This is an extremely violent treatment that no one in their right mind would use for HIV - it's just a last-resort treatment for fatal blood cancers that happened to have cured HIV in some patients.
You really should tell your partner if you are infected, on medication or not. You are still dependent on medicine for the rest of your life apart from these cases. So it still is a big deal, but it isn't a death warrant anymore.
Responsibility shouldn't be taught by deadly diseases, you could have said the same about antibiotics.
>> I think it's quite likely that at least one of these 5 people have... something in their body that could be transfected into another person's cells and cause an active HIV infection.
No, they definitely don't. It's well known[1] that people without detectable levels of HIV in their blood cannot transmit HIV to other people. That is true for people who are simply receiving normal treatments (see: https://www.nih.gov/news-events/news-releases/science-clear-...). It is certainly also true for these transplant recipients.
Edit:
[1]: Specifically, researchers have never observed transmission from someone with undetectable viral load, despite many large studies searching for such an event
What you've said is true, but I'd add that there are worrying number of HIV+ men that have stopped disclosing their status to sexual partners because they've heard that "undetectable = untransmissible." While that does seem to be true, there are a number of problems with this:
1. Not everyone takes their medications exactly as prescribed.
2. Lots of folks on antiretroviral therapy are not undetectable, or may move between undetectable and detectable over time.
It's important that people still disclose their status to sex partners.
A lot of misconceptions in this and other comments. To address the two most glaring ones:
> 1. Not everyone takes their medications exactly as prescribed.
That's irrelevant. Not only is there a fair amount of leeway in the standard dosing schedules (meaning that missing some doses does not actually cause a clinically meaningful impact), but the studies that demonstrate that U=U are based on real-world applications. Variability from adherence is already captured by the results.
> 2. Lots of folks on antiretroviral therapy are not undetectable, or may move between undetectable and detectable over time.
This is not true and based on an incorrect understanding of what "undetectable" signifies clinically. Once a person has durably achieved clinical undetectability under HAART, they do remain undetectable, as long as there is no prolonged disruption in treatment[0]. The most common reason for a disruption in treatment is an inability to access treatment - not something that happens without the person's full awareness.
People on Internet forums like HN like to get worked up about bogeymen like people intentionally not taking their medications, but actual clinical data shows that stuff is largely the realm of urban legends, not reality. And if you're that concerned about it, the answer is simple: PrEP prevents HIV with a near-100% efficacy, rendering the question "is this person undetectable?" moot.
[0] Emphasis on prolonged. Missing a few days, or even a week or two, does not cause HIV to become detectable again. These sorts of treatment interruptions are contraindicated, but for other unrelated clinical reasons, not because of the impact on viral load.
While you are right, I don't think any of this is an excuse for not sharing your status.
Yes we should remove the stigma around HIV and I am sympathetic towards those that have it and still deal with that stigma that very much exists within the gay community.
Myself I am on Prep, and while it is a near 100% it is not in fact 100%. And yes I know I can't get it from someone who is undetectable.
But I also know I had a situation where after hooking up with someone I found out they were undetectable. That made me feel uncomfortable, largely because he did not tell me. It immediately made me question, is this guy actually undetectable as he is claiming? Is he taking is medication properly? Is there something else he didn't tell me.
To be clear I have hooked up with people who have that information in their profile or they told me beforehand, but I have major issues with not being up front with that information if we are about to have sex. I would expect the same for any STD, testing positive for Covid, or any other thing that could have an impact on me.
> as long as there is no prolonged disruption in treatment
Which happens all the time. Treatment is significantly more burdensome and expensive than women taking birth control, for example, and we all know how accidents still happen.
Notice how you’re shifting the blame to the victim, who was knowingly put at risk. “It’s really your fault because you’re not on Prep.”
It’s just bizarre how worked up people get about not wanting to be honest with their sex partners. It’s basic human decency.
Birth control has way less leeway than the parent describes hiv treatment. Oral birth control fluctuates wildly and must be taken literally within the same hour or so every day. I don’t think birth control and hiv transmissibility are comparable cases here, because the potential for pregnancy and the potential for hiv infection don’t appear to work remotely similarly. I don’t personally have a horse in this race, I’m merely pointing out I think this comes off as not understanding pregnancy prevention, hiv treatment, or both.
No analogy is perfect. My point is that people go on and off HIV medication all the time for all sorts of reasons: costs, burden, side effects, etc. By comparison birth control is very easy. It’s an example how medicine can be effective, but still create risks in real life.
The parent poster says going off hiv medication doesn’t really happen outside of external circumstances and even when it does it takes weeks to cause a problem. This isn’t the same for birth control.
> there are worrying number of HIV+ men that have stopped disclosing their status to sexual partners because they've heard that "undetectable = untransmissible."
I thought that was the entire point of the “undetectable = untransmissible” campaign — freeing people from worrying about passing it to others and having to live with a scarlet letter, which is an incentive to get treated
> It’s important that people still disclose their status
Nobody is saying you should live with a scarlet letter. But you should disclose to people you're having sex with your status and let them make an informed decision.
Untreated HIV (usually) takes years to cause AIDS, and then takes months to years for you to die from it. Before you have AIDS, you can still start treatment, and can still enjoy a long life afterwards. That being said though, the earlier you start treatment, the better.
So yes, there are still strong incentives to get tested, but people still don't get tested when having HIV is criminalized.
Yes okay, so you should have a scarlet letter only visible to people with whom you have a class of relationship that is particularly fundamental for human happiness.
If you’re having consensual sex, you should be able to discuss the risks with your sex partner. It isn’t a scarlet letter to discuss the fact that you have a disease which is understood to be currently noncommunicable. It’s discussed openly in communities with high risk factors. Keeping known risk factors from your partners is a betrayal of their trust effectively on par with violation of their consent. It denies them the possibility to even determine whether they understand the risks they’re taking. It further denies them the ability to evaluate that risk over time as their partners’ input to that risk might evolve.
None of this is specific to HIV! This is basic interpersonal responsibility as taught to middle school children basically everywhere that doesn’t have a severely toxic anti-sex culture. Clear and honest communication about risk of disease is essential to healthy, consensual sex. And that’s been known since at least when I was a teenager well back into the last century.
This is a perfect counterexample for the flawed logic of the argument put forth by another commenter above, which appears in marketing materials for drug companies in American media, frighteningly.
In the first year after achieving VL undetectability, 354/1386 (25.5%) patients experienced low-level VL rebound, the remaining patients maintained consistent undetectability. Low-level rebound occurred less commonly with non-nucleoside reverse transcriptase inhibitor (NNRTI)-based HAART than with other regimens (P = 0.01). Over median 2.2 (range 0.0-7.4) years of subsequent follow-up, 86 (6.2%) patients experienced virological failure, corresponding to 2.30 failures per 100 person-years (95% confidence interval [CI] 1.82-2.79). Independent predictors of virological failure included low-level rebound during the first year after achieving undetectability relative to consistent undetectability (rate ratio [RR] 2.18, 95%0 CI 1.15-4.10), female gender (RR 1.79, 95% CI 1.12-2.85) and receiving a ritonavir-boosted protease inhibitor (Pl/r) relative to NNRTI-based HAART (RR 1.88, 95% CI 1.02-3.46).
> In the first year after achieving VL undetectability...
I'm gathering from your comments that you don't have a clinical background in HIV research (because if you did, you would not be posting this as a reply).
Not only does your link not prove what you think it does, but it actually says the exact opposite: once a patient has durably achieved clinical undetectability under HAART, they do remain undetectable, even when using older generations of drugs that are no longer first-line treatments. It even states that in the conclusion: " Patients on first-line HAART who maintain consistent VL undetectability for 1 year have a low risk of subsequent virological failure."
To spell it out: the mistake you're making is that you're looking at a paper that studies treatment-naive patients and whether or not they durably achieve undetectability, whereas what we're talking about is patients who have already durably achieved undetectability.
So the paper you linked isn't particularly relevant to our conversation, because it's studying a completely unrelated endpoint, but by coincidence, it does actually corroborate the point I was making.
What you quoted does not support your point. “have a low risk of subsequent virological failure"
Low risk is not zero risk. Also the actual population of people who durably achieved undetectability is effectively a true Scotsman argument in that you reject people who seemed to achieve it who then became detectable again. We don’t have long term data saying all people who are undetectable for N years are undetectable for 40 years because the treatments aren’t that old. All we can do is extrapolate and people who are undetectable for even 4 years have become detectable.
Newer treatments look promising but they have even less long term data to extrapolate from. And of course things look even worse when people stop taking treatment for various reasons.
If you’re trying to use it as a scientific term then actually apply the term correctly. They specifically mention failures in such people in the actual paper though do indicate it’s a low risk for that population:
They note risk factors for increased viral load include include illness or vaccination etc. The intent may be to remove people who have regular failures but the definition isn’t purely based on their underlying medical condition. With that 1 year as a benchmark you’re excluding people who happened to experience such risk factors while excluding people who have yet to experience them.
> If you’re trying to use it as a scientific term then actually apply the term correctly.
Your comments in this thread are a very good example of the aphorism "a little knowledge is a dangerous thing". As I mentioned above, it's pretty clear that you don't have a clinical background in HIV, because you're mixing up terms that have precise clinical definitions and drawing conclusions that are not only not warranted, but actively contradicted by the data.
There are a lot of incorrect statements or mistaken assumptions that you're building on here. I've pointed out a few of them already, but without the contextual domain knowledge, it would be difficult to correct them all in a way that's accessible to a lay audience. It certainly would not be possible in the scope of an HN comment.
As a general note: it's okay not to be an expert in a given field, but in that case, please keep that in mind when discussing it. The ability to find information which appears intelligible does not in se imply the necessary knowledge to contextualize and interpret that information correctly. That's particularly true when talking about information written for an incredibly specialized audience - even most clinicians would not be expected to read a paper on this topic, because HIV is a fairly unique subfield that requires a lot of domain-specific knowledge.
I have done professional work with HIV, not in the last 4 years but I doubt much has changed.
You’re repeatedly ignoring data showing you are wrong and in this case dangerously wrong. Read the damn paper I linked or any of several others which show the same thing. HAART is good but not perfect.
That's rather vague wording, so I'm not really sure what I'm supposed to make of that.
As I've pointed out multiple times, your comments include rather basic mistakes in terminology which demonstrate a lack of clinical familiarity with the topic at hand. Those misunderstandings are causing you to make make inferences that are not valid. You're reading this as "ignoring data showing [I am] wrong", but in reality, it's that the data simply doesn't say what you think it does.
If that isn't convincing, you can look at it from the other end entirely: the original claim you made (that "it’s important that people still disclose their status" because "having undetectable levels on day 1 doesn’t mean you have undetectable levels on day X and people don’t test every single day") is a conclusion that is soundly rejected by both public health experts and epidemiologists who specialize in HIV treatment and prevention.
As a rule of thumb: if you're citing orthodox methodology and research to make extremely heterodox claims, that's a good sign that you've made a mistake somewhere along the line.
That's as much time as I'm really going to spend discussing on a comment thread that I now see is inaccessible because the original comment is now flagged dead (and, frankly, for good reason).
I guess there’s a difference between a mathematical proof and practical, real life truth. Multiple studies have looked for transmission across tens of thousands of unprotected penetrative sex acts. There’s also a solid theoretical backing to the concept - it lines up with how we think HIV transmission works.
So it’s a bit like saying maybe there’s Bigfoot out there. Sure, maybe, but we have a pretty good reason to think there isn’t. For practical purposes no one should assume big foot is out there.
I'm not saying they could transmit though sex, I'm saying they could be caused to transmit through what is essentially viral cloning, by taking either a cell (or probably many cells, because the recipient has an immune system) containing proviral DNA (i.e. the DNA created by HIV's reverse transcription mechanism), and putting it into the recipient, or by taking the HIV proviral DNA from that cell and transfecting cells of the recipient with it, similar to how you can clone a polio virus by transfecting a cell with the DNA of polio, even though polio is an RNA virus. This has been done by Vincent Racaniello using early DNA sequencing techniques, and could be tested in an animal because of the Gain of Function'd mouse model he made. I can't remember anyone being able to create an animal model for HIV though...
Well in that case I hope no one is out there transplanting cells from these people into other people. I can’t imagine why anyone would do that. It seems to me like this should still count as curing someone.
Well, I think being precise in virology is a good thing. For example being infected with SARS-CoV-2 and having the disease COVID-19 are not exactly the same thing, and matter quite a bit when writing a prescription for Paxlovid. You can't (or aren't supposed to) write off-label prescriptions for EUA drugs, so it does matter. Apparently they changed the EUA recently though, and Internet rules lawyers think they can prescribe it to people who don't have COVID-19 at all, so it might not matter at this point.
I don't know much about this, but I read that some primates have endemic SIV and don't get sick, whereas some other species of primate will die of AIDS after exposure to SIV.
For example, Wikipedia on SIV says that ~90% of female African green monkeys (vervets) have SIV, and don't get AIDS.
From there one imagines that a primate species on first exposure to the virus has it as a deadly disease, but sometimes they evolve a resistance to getting sick from it, without eradicating the virus.
Apologies, I know nothing about this at all, but why is it more surprising for HIV than other viral diseases that do have successful cures (like hepatitis C)?
In simple terms, rather than always using a cell it takes over to make as many copies of itself as possible which then circulate and get dealt with by the (possibly boosted) immune system, HIV can hide itself in human DNA and let the normal human cell division process create a reservoir of apparently normal human cells which can produce copies of the virus in future
k thanks, so I guess you've studied this for as long as it took to write 129 words on the subject. I am going to have to be way more interested in the actual people who are studying and experimenting with this at this point, I can't allocate any interest at all in your 129 word paper on the subject.
1. You completely missed the point of the article. The (formerly) HIV-positive patient RECEIVED a donation.
2. HIV is already screened for in blood donations. (Whole blood donations also come with a long list of questions which gauge for some things you might consider "risky behavior", like injection drug use or sexual contact with sex workers.)
3. With proper treatment, most HIV patients today have a non-detectable viral load of HIV in their blood. This doesn't mean that they absolutely CANNOT transmit the virus, but that the quantity of virus is vanishingly small. To quote the NIH[0]:
> While it is still possible to transmit HIV to others during [Chronic HIV infection], people who take ART exactly as prescribed and maintain an undetectable viral load have effectively no risk of transmitting HIV to an HIV-negative partner through sex.
I have a hard time imagining a future where allogenic stem cell transplants are used to treat HIV. The procedures are incredibly risky and carry long term consequences (and in many cases, like mine, also unbearably painful for weeks).
To me, the most likely practical consequence of these findings is to spur on interest in using CRISPR (or other in-vivo genetic modification strategies) to alter the genome of an HIV patient to be "immune" to HIV. (A similar idea is used in treatment of some blood cancers. Chase the rabbit-hole of "CAR T Cell therapy" to get started.)