Anti-“HIV” drugs are not specific to “HIV”—exhibit n for some decently large n
We’re now using “anti-HIV” drugs as PrEP for OTHER INFECTIONS
This will be a very short post; however, I came across this study and I think it’s relevant to our many discussions regarding the non-specificity of “anti-HIV” drugs. We will be briefly looking at a study that examines the potential use of Truvada for PrEP against hepatitis B virus.
How on earth does anyone still believe the narrative that these drugs are somehow the holy grail of biomedical engineering due to their astounding specificity to “HIV”?
Oral emtricitabine-tenofovir disoproxil fumarate (F/TDF) for HIV pre-exposure prophylaxis (PrEP) demonstrates dual potential through antiviral activity against hepatitis B virus (HBV). While F/TDF lacks activity against hepatitis C virus (HCV), the use of F/TDF for HIV PrEP may elevate HCV risk through risk compensation. This study aims to investigate HBV/HCV incidence among men who have sex with men (MSM) using F/TDF-based HIV PrEP, addressing evidence gaps in low- and middle-income countries.
Interesting how they’re prescribing Truvada, a nephrotoxic medication, to patients with an infection that damages the liver. Let’s trade damage to one organ for damage to another, perhaps?
Results
The CROPrEP cohort prospectively recruited 1023 F/TDF users and 507 F/TDF non-users at baseline. This secondary analysis included 259 F/TDF users and 120 non-users identified as HBV-susceptible at baseline. At the 12-month of follow-up, no incident HBV infections occurred in the F/TDF users group, and only one incident HBV infection occurred in the F/TDF non-users group. The incidence of new HBV infections was 0.00/100 person-years (PY) [95% confidence interval (CI): 0.00–1.32] among HBV-susceptible F/TDF users and 0.77/100 PY (95% CI: 0.02–4.20) among HBV-susceptible F/TDF non-users. HBV incidence was reduced with F/TDF compared with no F/TDF [adjusted incidence rate ratio (aIRR): 0.00; 95% CI: 0.00–0.00]. HCV incidence among F/TDF users and non-users was 0.31/100 PY (95% CI: 0.06–0.90) and 0.00/100 PY (95% CI: 0.00–0.74) after 12 months, respectively. HCV incidence was lower in F/TDF non-users than in F/TDF users (aIRR: 0.00; 95% CI: 0.00–0.25).
I’m including this paragraph for a reason, and that reason is their results: No HBV infections occurred in the treated group. The sample size is admittedly not huge, but it’s sufficient to extrapolate what might happen were more participants included.
Why is this important? Well, remember the perfect lenacapavir results in the initial trial that resulted in no seroconversions among the treated group? (There was a later trial that was not so perfect, but that is not germane at the moment.) That trial was widely reported upon; might we finally have a therapeutic that functions effectively as a vaccine? Of course the implication was that lenacapavir, and other drugs, is so wildly specific to “HIV.” However, would the results of the HBV PrEP study be used to imply that Truvada is “highly specific” to HBV? I think not. (Also, we know the toxicities of Truvada; might similar toxicities emerge with lenacapavir?)
Perhaps these types of studies might end up finally dismantling the HIV AIDS story; if these drugs continue to be prescribed to ever more conditions that have nothing to do with “HIV,” might the public soon begin to actually question the “HIV” absurdities? A girl can hope.
I think one of the tricks used in these kinds of papers is that they're intentionally using obscuring language. That being said, I doubt their sample sizes are large enough to be really meaningful. BUT, my guess is they will say this anti-HepB activity is because HepB is said to use reverse transcription activity also. But to me the infuriating thing is that the complex edifice of virology obscures that's likely actually going on at a cellular level. Meaning I think these drugs are doing nothing more than interfering with signals read as these viruses. It's all smoke and mirrors.
Keep hoping, girl…and this boy will keep hoping, too ;-)