We have a new problem with PrEP.

PrEP may be “masking” “true positives” during “acute infection”

This is a highly preliminary report on a phenomenon that is very curious indeed. I’ve been looking into “acute retroviral syndrome,” which is a “flu-like illness” that occurs “within weeks” of “HIV” infection and has, anecdotally, wildly varying symptomatic presentation, and does not occur in every individual that eventually “seroconverts.” We don’t even know in what proportion of individuals it occurs—the estimate I obtained from the NIH is “40-90%,” a confidence interval so wide as to be totally useless, and doesn’t take into account the possibility that this totally nonspecific clinical manifestation of illness could have another cause, like the actual “flu” (including the many “influenza like illnesses”) or a reaction to some kind of toxicity.

However, this post is not about acute retroviral syndrome, although I will be reporting on this very soon. It’s quite the mess. In my digging into this syndrome, I came across the following article from JAIDS published in 2019:

Positive or Not, That is the Question: HIV Testing for Individuals on Pre-Exposure Prophylaxis (PrEP)

Here’s the opening (emphasis mine throughout):

We report a case of an individual exposed to HIV around the time of pre-exposure prophylaxis (PrEP) initiation where detection of HIV-1 RNA and initial diagnosis were delayed. PrEP has the potential to alter the detection of biomarkers of early and acute infection leading to potential confusion in interpretation of HIV status and delayed treatment of similar cases in settings where PrEP is delivered.

Well, this has my attention. (Also—delayed treatment? They’re already on two “anti HIV” drugs; I guess we can’t possibly miss the opportunity to add a third drug to the regimen. Some ARVs themselves, like Dovato, only contain two drugs. This is all so ridiculous.)

But what I’m really interested in is the potential of PrEP to “alter the detection of bio markers of early and acute infection.” If it has the potential to alter these bio markers, what else can PrEP and ARVs do throughout the course of “infection?” The following quote is long, but it presents an interesting case study, so I encourage you to pay attention to the details below.

A 31-year-old male presented to a New York City Department of Health clinic for PrEP assessment. A 3rd generation rapid HIV and pooled nucleic acid amplification (NAAT) tests were negative at that time.

[…]

The patient was started on tenofovir-emtricitabine (TDF/FTC) at this visit and was given a 30-day supply. A 4^th generation HIV test (Abbott Architect Ag/Ab Combo), gonorrhea and chlamydia from three sites, syphilis, and hepatitis (A, B, C) were negative.

Twenty-eight days later the patient returned to the clinic, reporting 100% TDF/FTC adherence. At that time, Abbott HIV Ag/Ab was reactive with a signal to cutoff ratio (s/co) of 1.03 (Reactive >1.0). Supplemental testing was performed with the Geenius^™ HIV1/2 Confirmatory Assay (Geenius, Bio-Rad, Marne la Coquette, France) and was negative (See Figure 1). A qualitative HIV-1 RNA test was sent to the New York State DOH (NYSDOH). These results prompted re-testing four days later at which point the Abbott Combo s/co was 0.95, interpreted as “negative,” as was a qualitative DNA/RNA PCR (COBAS-Qualitative, AmpliPrep/TaqMan HIV-1 Qual Test). The virus was detected, however, using a quantitative test, COBAS AmpliPrep/TaqMan HIV-1 Test kit, with HIV-1 RNA level below the lower limit of detection (<20 copies/mL). At this point, Dolutegravir was added to the regimen.

Okay, so this shouldn’t be unfamiliar to most HIV AIDS critics. We’ve heard many stories about inconsistent test results, although they’re not exactly advertised. Also, how was the “virus detected?” Per the mainstream, “below the limit of detection” means they can’t find the “virus.” Details are not given in this paper, but I looked up the test they use to determine that the “virus was present” and it is simply a DNA amplification technique. This makes no sense; it isn’t even circular reasoning; it contradicts the mainstream model, as I’ll explain in my conclusion. Moving on. Here are the results of his follow up testing and his eventual medical fate; we’ll move on to the broader implications after this.

HIV testing was repeated two weeks later. Abbott Combo was reactive (s/co = 1.3), Geenius was indeterminate (positive for gp41 only), COBAS-Quantitative was not detected. However, COBAS-Qualitative was positive. The initial qualitative HIV-1 RNA from day 28 post-PrEP initiation ultimately returned positive. The patient was switched to a once-daily fixed-dose combination antiretroviral regimen and continues to have an undetectable HIV-1 RNA level. A GenoSure archive (GenoSure, Monogram Biosciences, San Francisco, California, USA) returned with insufficient HIV infected cells or cell-associated DNA targets to amplify the virus for assessment of mutations.

If you’ve read this carefully, you will notice that at no point did this patient ever exhibit a “viral load,” which is curious because it is meant to be in the millions during “acute infection.” (How do they know this? I’ll get into this soon, but the studies are underwhelming.) Could this possibly because these tests don’t actually detect an infectious agent at all? Of course, the study authors didn’t consider this possibility, but the explanation they present is itself quite devastating to the HIV AIDS paradigm. “To date, a comprehensive evaluation of how PrEP could impact diagnosis of acute and early HIV infection has not been fully completed.”

Several studies have shown that patients who acquire HIV while adherent to PrEP can have low or undetectable viral loads. Suppression of the viral load could plausibly result in false negative results during Fiebig stages II and III. PrEP thus has the potential to alter the natural history of disease-causing a failure of the current testing algorithm. While this case most likely does not represent a failure of PrEP given the patient’s exposures prior to and in the first week after PrEP initiation before optimal drug levels could be achieved, there have been three well-publicized cases of individuals acquiring HIV while on PrEP.

I wonder how many non-publicized cases have occurred, especially given the widespread lack of follow up and the fact that many people who start PrEP discontinue it.

Another question, and in my opinion the most important one: if PrEP has the potential to cause “low or undetectable viral loads” during “acute infection,” how then does the patient manage to “seroconvert” at all? According to the mainstream, the “viral load” (typically measured using PCR, but other methods may be employed) is an accurate reflection of the viral burden, or the actual amount of “HIV” in the blood, so how, logically, can an individual with no virus present possibly develop an antibody response to said virus? How on earth do they “seroconvert?” Could these drugs be altering bio markers that have nothing to do with “HIV” at all? It’s an intriguing possibility with potentially enormous implications.

As I said, this is a preliminary report, but I will be investigating this, as well as “acute retroviral syndrome,” much more deeply in the weeks to come. If you have any ideas or questions, let me know in the comments!

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