We’ve seen the narrative that PrEP failure is “rare,” with such examples as the following:
Has Anyone Gotten HIV When They Were on PrEP?
You can read about all eleven PrEP failures in the link above, and I’ll be doing a deep dive into each of these cases soon, because they’re really illuminating. The story we are meant to believe is that PrEP is perfect, and that only eleven people in the world acquired “HIV” while on PrEP; but of course we know it is not true given the dozens of seroconversions in the iPrEx PrEP study and other studies. However, I have recently come across the following paper, which I will be reviewing in detail very soon, and it is very interesting. Here’s the link to the piece:
Fourth-Generation HIV Rapid Tests: Enhanced Sensitivity and Reduced Diagnostic
And here is the money quote:Window for HIV-1 Primary Infection Screening (emphasis mine):
Of note, six of the 183 serum samples included matched four cases of HIV infection among TDF/FTC PrEP users, in all cases due to low treatment adherence. Reported time of infection was available for two of them (three samples) and ranged from 20 to 30 days. Both rapid tests were antibody-reactive on all six serum samples.
Six out of 183? That’s actually quite a lot, when we consider the incredibly low transmissibility of “HIV,” per the mainstream. Were these “seroconversions” among the eleven mentioned at the top? I’m guessing not. And this is just one paper. Never mind the fully 34 seroconversions that occurred in just one study. So much for 99% effective. So my question to you is: what is really going on with PrEP? What is it actually doing to people? What signals might it be masking? Recall that we recently discussed the oddity of a patient on PrEP that allegedly contracted “HIV” with no measurable viral load, yet developing an antibody response? What are these antibodies reacting to? It can’t be “HIV.”
So what is really going on with PrEP? Are PrEP failures really “rare?” It sure doesn’t sound like it. And what is really going on with “HIV,” if a person can somehow mount an antibody response to an undetectable “virus?”
I’d love to hear your thoughts on this.
Thanks, Miss Rebecca.
Scientifically, what is meant by the term "sero-conversion?" I think we are supposed to believe that certain proteins of HIV origin were present in a given individual's blood sample prior to "treatment," and absent following treatment. And, presumably, that antibody detection (Western or ELISA) was the indirect method used to make the claim of "sero-conversion."
Assuming their "sero-conversion" biological model were accurate, detection (or not) of a given protein is inconclusive, as protein abundance varies widely over time, depending on (largely unknown) biological mechanisms controlling or regulating protein expression levels.
Also, antibody detection is an experimental method fraught with variability and is a procedure involving many components and steps, any of which can affect results outcome.
Antibodies (both primary and secondary) vary widely, and, as biological molecules, have limited lifespans. Concentration used for each antibody must be experimentally determined- rarely, if ever, done. Similarly, the detection molecule has wide variability and short lifespans.
Currently, the digital signal capture machines and the reliance on software for amplification and interpretation of signal is the greatest source of error. But even prior to these digital machines, few procedures were more problematic than antibody detection of (claimed) specific proteins.
So, while I understand the general discussion, the fundamental scientific assumptions underlying manufacturer claims range from refuted hypotheses to sheer science fiction. How does one argue against pseudoscience using a scientific reference?- it can't really be done.
"HIV"