Treatment of "HIV" during "acute infection"?

"Mathematically modeling" the mysterious "reservoir"

The following appeared today in Poz magazine, and it’s a doozy, opening as it does with a nifty cartoon of “HIV” inside a CD4+ T cell (you’ll have to click the link to see it as I’m sure the image is copyrighted):

Early HIV Treatment Shrinks Viral Reservoir

Let’s begin with the pull quote: “Starting antiretrovirals during acute infection leads to more rapid decay of the viral reservoir, which could improve prospects for a functional cure.”

Well, before we even begin, we notice that they refer to “acute infection,” which is purported to be that time in between initial “infection” and “seroconversion,” which is the point at which antibodies to “HIV” are meant to show up on diagnostic tests. There is a problem here right out of the gate, as even per the mainstream, there is no reliable way to determine if a patient is experiencing “acute ‘HIV’ infection.” The reason for this is that “acute infection” can be, but often is not, marked by a highly nonspecific “flu-like” illness with wildly varying symptoms, and there is no real way to determine if said illness has anything to do with “HIV” (even per the mainstream). As I reported previously, it is apparently possible to mount an antibody response in the absence of any measurable “viral load.” Theoretically, “acute infection” could be determined by measuring “viral load,” except when it can’t. It’s a completely bankrupt concept.

Let’s get into the article:

People with HIV who start antiretroviral treatment very soon after infection experience a faster decline in the size of the viral reservoir in CD4 T cells, according to study findings reported in a recent preprint. While early treatment usually does not prevent viral rebound after stopping antiretrovirals, a smaller reservoir could raise the likelihood of long-term remission in cure studies.

Once again, we come back to the pesky “reservoir” that has been troubling “HIV” researchers from the beginning. Despite the advances in “life saving drugs” over the years, neither the vaccine nor the cure that were promised by 1986 have yet to eventuate. Yet the possibility that failure after failure may indicate a fundamental misunderstanding of AIDS is never considered.

The only way to tell for sure whether an intervention leads to long-term remission is to stop ART with careful monitoring, known as an analytic treatment interruption. But mathematical modeling can shed light on viral dynamics and control without the attendant risk of disease progression and HIV transmission while off antiretrovirals. Modeling data “would be immensely useful in future HIV cure trials to compare expected reservoir decay rates in comparison to curative interventions and allow generalizability of findings to a more global population of people with HIV treated during acute or chronic infection,” according to the researchers.

Here we go with the mathematical modeling again. I know a little bit about that subject, and I’d like to take a moment to remind you that mathematical models cannot prove anything. A mathematical model can, at best, quantify an effect that the modeler has already assumed to be true. If a model tells you that a variable has a certain effect, it is because the modeler input it assuming it to have said effect. So if this model wants to prove that “shrinking the reservoir” has long term positive clinical effects, it must necessarily assume that it does. That’s how models work. Let’s see what else they have to say about these mathematical models.

Barbehenn’s team developed a novel mathematical model to predict reservoir decay using a test that measures proviral DNA in peripheral CD4 cells in circulating blood. They looked at both intact, or replication-competent provirus that can produce new infectious viral particles and defective proviral DNA that can’t produce infectious virus. Study findings were presented at the 2023 International AIDS Society Conference on HIV Science and have now been reported in a preprint that has not yet been peer reviewed.

Notice that the preprint of the paper has not yet been peer-reviewed, yet the results are somehow worthy of a piece in Poz. The second sentence is interesting. They refer to “replication competent provirus;” this is not the same as an isolated virus but instead refers to the genetic material as incorporated into the genome of a host cell. So already, this isn’t a “free viral particle,” it is part of the host cell’s genome. I’m sure you can imagine the problems with this approach—how do we know where this genetic material actually comes from?

The researchers collected more than 500 blood samples over time from 67 people in the UCSF Treat Acute HIV cohort who started ART during acute infection, or up to 100 days after the estimated date of infection. Most were gay or bisexual men, reflecting the local epidemic. About 40% reported prior pre-exposure prophylaxis (PrEP) use, and 20% reported PrEP use in the past 10 days. Those who reported PrEP use had a lower baseline viral load but not a smaller viral reservoir. All participants were followed for six months. About two thirds joined the UCSF SCOPE HIV cohort and received additional follow-up.

Well, that caught my attention. A nontrivial proportion of participants that “seroconverted” had been on PrEP—but guys, I thought PrEP was more than 99% effective? Oops. Also, is the definition of “acute infection” intentionally vague? “Up to 100 days after the estimated date of infection?” How many people, “HIV positive” or not, experience a flu-like illness within any given 100 day period? What a useless definition. Also, followed for six months? For a viral disease that supposedly takes over ten years to even show up? Let’s look at their actual results.

The models showed biphasic decline of proviral DNA out to one year. During the first phase of decay, lasting up to five weeks, there was a rapid, steep decrease in intact DNA followed by a much slower decline during the second phase. The first-phase decline was comparable to previous estimates for people who started ART during chronic infection, but the second phase decay was about five times faster compared with prior estimates.

The models showed decay of proviral DNA. Translation: this decay was not directly observed in the patients, but inferred from a model. I’d also be interested in an answer to the question as to what the actual clinical significance of this “second phase decay” actually is. The research into this “virus” has become abstracted to the point of near total uselessness.

This piece is already way too long and filled with yet more abstracted nonsense; let’s see if we can cut to the chase.

The initial rapid decline in proviral DNA in the first phase is thought to reflect the death of infected CD4 cells after ART initiation during either acute or chronic infection. But people who start treatment early have less exhausted immune cells and more intact immune responses, the authors noted. These findings could help personalize HIV cure strategies, suggesting that people who start antiretrovirals very soon after infection may achieve remission more easily, while those who start during chronic infection may need additional interventions.

“People who start treatment early have less exhausted immune cells”? Here we go with the anthropomorphization of the interaction between “HIV” and the immune system. It’s so tiresome. Seriously, though—what have we learned from this piece and the study it reports on? Nothing new, as far as I can tell. The researchers take a previously held assumption—in this case, that early treatment “shrinks the reservoir” (what effect this has on health is unclear)—and extrapolate wildly to posit that it would have an even greater effect if administered during “acute infection,” which unfortunately remains nearly impossible to diagnose in real time, and we all know the reason, and that is that the whole idea of “acute ‘HIV’ infection” is a fairy tale that will never be proven, and that is because the HIV AIDS story has long since been falsified. No amount of cute cartoons and animations can hide the truth of the matter. And that’s all I have to say about that.

Let me know what you think in the comments!