“Four Decades of HIV”

Fascinating review article

The review article “Four Decades of HIV: Global Trends, Testing Assays, Treatment, and Challenges,” by Muhammad Haris and Rizwan Abbas, was published January 4, 2024 online at the journal Zoonoses. Here is a short online description of that article:

Four Decades of HIV

There are a few items of interest in the full article that I’ll be drawing your attention to. I’ll first explain the general setup of the article. After a brief introduction and a “Historical Outline,” we move into a discussion of HIV testing (from first- all the way to fifth-generation assays). Types of tests are discussed, as well as “testing strategies.” From there, we move on to “Global Trends in HIV Prevalence” (it’s always “HIV,” isn’t it, never AIDS? If I were a person with HIV-negative AIDS, I’d be annoyed). This section is fascinating, and it includes, for different countries and regions, the actual uptake of antiretroviral therapy as well as the PLHIV (people living with HIV) burden. This is followed by a discussion of treatment options, including a handy chart of approved types of ARVs by category. The most ominous section comes next, and it is titled “Functional Cure.” Finally, we have a summary of “Challenges,” and a conclusion. Let’s dive in.

The introduction says about what you’d expect it to say, so I won’t spend time on it, except to note that the authors give a warp speed summary of the drug development, leaving out AZT entirely. Let’s move on to the section on HIV testing. After all, this epidemic is an epidemic of test results at this point—not of clinical illness—so the test is critical to the epidemic’s very existence, in some sense. In the preamble, it states: “The subsequent use of fourth- and fifth-generation systems for HIV detection accelerates the testing process and significantly reduces the detection window.” (Emphasis mine.) Remember that line; it’s important and we’ll come back to it shortly.

To quickly summarize the different assay types, the so-called “first-generation assays” included the infamous ELISA antibody test, the Western Blot “confirmatory” test, and the “HTLV-III Immunofluorescence Assay.” (There’s a blast from the past; we haven’t heard “HTLV-III” since the early 80s.) The tests were developed to screen the blood supply, and were deemed to be quite sensitive, meaning there would potentially be many false positive results. However, there were also concerns about the lack of sensitivity during to “window period” between “acquisition of HIV” and antibody production, since the test only detected antibodies and no antigens. The second- and third-generation assays included antigens as well as antibodies, focusing on the p24 “HIV” antigen (there is a section in my book explaining that p24 is not exclusive to “HIV”). These tests also included the ability to detect HIV-2 (which is alleged to be the “less virulent” strain that remains mysteriously almost entirely confined to the continent of Africa), and enabled the detection of antibodies earlier than did the first-generation tests. Finally, the fourth- and fifth-generation tests shortened the “window period” to 2 weeks. From the article:

However, in 2014 a single algorithm was finalized to determine whether the infected person had antibodies to HIV-1 or HIV-2, followed by HIV-1 RNA PCR amplification.

Ah, there it is. After years of not using PCR for diagnosis, because as we know it amplifies all sorts of genetic material supposedly related to HIV (but not necessarily—remember false positive viral load tests?) and is therefore unsuitable to diagnose anything, now PCR is being incorporated into diagnosis. I’d like to know the official explanation as to why, because this particular review article is hand-wavy about the rationale. But this ought to raise some huge red flags. Kary Mullis must be rolling over in his grave.

So, we can see that not much has really changed in any significant way when it comes to how these tests work. They are still detecting antibodies to, and antigens associated with, a pathogen that has never been proven to be isolated.

There is also a short section on counting T cells, which we know about already. What I found interesting was the chart comparing sensitivity and specificity of the five generations of HIV tests. Recall that sensitivity refers to the ability to find something elusive; high sensitivity guarantees that the test will (at least) occasionally label patients without the condition being tested for as falsely having it. Specificity, however, refers to being able to find the thing being tested for to the exclusion of anything not being tested for. High specificity, for that reason, might falsely leave out true cases. So, for the first-generation tests, specificity is listed as 95-98% and sensitivity at 99%. You’ll notice that the sensitivity never goes down, meaning that we’re not eliminating any false positives. Second-generation tests list a specificity of 99% and a sensitivity of 99.5%. Third-generation has 99.5% specificity and again, 99.5% sensitivity. The fourth-generation tests are claimed to be 99.5% specific and 99.8% sensitive. Finally, the current generation of tests lists 99.5% specificity and an astounding 100% sensitivity. This means that no positive test is left behind. Do with this information what you will, but the official numbers don’t exactly show a dramatically better testing methodology than we had in 1985. I also find it interesting how incredibly exact the numbers are—99.5% to 99.8% is not exactly that impressive a leap. Of course there are good reasons to doubt those numbers entirely, but that is a topic for another day.

The next section discusses testing strategies. They discuss three: facility-based testing, which could cover going to a doctor or clinic; community-based testing, such as testing in the workplace or at a pop-up or mobile clinic; and self-testing. The benefits and drawbacks are listed for each, but I’d like to move on to the “Global Trends in HIV Prevalence” section.

The following sentence is actually from the section on self testing, but it’s relevant so I’ll repeat it here: “In addition to the availability of testing kits, approximately 30% of all individuals with HIV are still unaware of their serostatus.” Thirty percent. How was “HIV AIDS” reduced to a “chronic, manageable condition” worldwide if almost a third of people don’t even know they have it and are therefore not accessing treatment?

Global prevalence is separated into the categories of Asia, Africa, and Europe, U.S. and the Caribbean (one section for the three). They talk some about risk groups, but the only thing that really jumped out at me was the statistic about China, a country of over a billion people. The 2021 HIV prevalence in that population was 1.053 million, which is fewer than the number in the U.S. by a factor of three. That figure represents only 0.1% of the population of China. This observation supports Dr. Henry Bauer’s observation that, regardless of risk status, Asians test HIV-positive at a much lower rate than do all other racial groups.

The really interesting part of the story, though, are the statistics involving “retention in care” of these so-called HIV-positives. We are told repeatedly that the reason AIDS is no longer the big scary problem it was 35 years ago is because of these amazing drugs that came out that reduced it to a “chronic manageable condition.” For that to be the case, we must have the vast majority of those eligible to be “retained in care” on those drugs. Given that a whopping 30% don’t even know their status, I’m suspicious.

We are given a chart of thirty countries from all regions listed, including their “PLHIV burden” (people living with HIV) as well as the number, and percentage, of those “retained in care.” Remember, this only applies to those that know their status. Those figures range from a high of 94% in the three African countries of Zimbabwe, Kenya, and Tanzania, to a low of 9% in Afghanistan. The total figure for percentage retained in care is approximately 67% across these thirty countries. Again, I ask: Where is the massive AIDS crisis? Not “HIV disease.”

The last item of interest is an explanation about the classification of drugs. Hilariously, this section opens with the following: “The mortalities and morbidities due to HIV infection have been drastically reduced with the use of ART and improved immunity of infected individuals since 1996.” How come AIDS deaths started dropping several years prior to 1996?

Discussing drug development, they state that “Antibody development was a major concern to treat HIV, however, various trials of several HIV vaccine candidates and two specific trials of antibody-mediated control revealed no effectiveness in HIV acquisition.” Oh, snap. One thing that stood out to me about this review article was how little time was spent discussing vaccine development, probably because everyone knows that a vaccine will never eventuate.

Regardless, there is a rather useful description of the following drug subtypes: nucleoside reverse transcriptase inhibitors (NRTI), non-nucleoside reverse transcriptase inhibitors (NNRTI), integrase strand transfer inhibitors (INSTI), protease inhibitors (PI), and entry inhibitors (EI). We know that NRTIs were first developed and include our old friend AZT, and we also know that they block DNA synthesis and therefore halt cell division, which is euphemistically referred to as “binding to reverse transcriptase and inhibiting viral synthesis.” Viral is not the only type of synthesis they inhibit, which is why they have such a terrible side effect profile.

There is a very useful chart that lists all currently FDA-approved medications by type and also lists their year of approval. We begin with AZT, an NRTI approved in 1987, and conclude with cabotegravir/rilpivirine, INSTIs approved in 2021. It is worth noting that all three PrEP drugs—TDF, TAF, and emtricitabine—are NRTIs.

Finally, we come to the section “Functional Cure.” I suspect this is referring to the use of drugs for “viral suppression” in place of a cure, and to PrEP as a kind of vaccine. It begins by stating “Several mediations to stimulate and promote functional cure of HIV have been revealed and explored with the goal to render the ART and drugs for a prolonged period.” This sentence is confusing. Anyway, these methods for a “functional cure” seem to involve targeting the “reservoir” of HIV, though it fails to explain exactly what this “reservoir” is. The methods include “activation and death of dormant virus.” The authors state: “A cure that decreases the frequency by 45-50% with every cure could be directed and managed twice to decrease the frequency to one-quarter of the previous amount. This type of cure would need to be given 10 times to decrease the frequency of HIV detection up to 1000-fold.” I’m exhausted after reading that. Also, if a “cure” needs to be given ten times, is it truly a cure?

We also have “cell subset targeting,” a “nominally lethal method to reservoir decline.” There is “gene silencing,” additionally, which uses CRISPR technology—enough said. Finally, we have “nano particles targeting viral function.” None of these is a cure for anything, 38 years after the 1986 timeline we were initially given for a “cure.”

The article concludes with a list of challenges, including “ARV drug resistance,” “Global concern,” “Vaccine development,” and “Co-morbidities and aging.” These say exactly what you’d expect them to say. I do think it’s fascinating that “Vaccine development” is one paragraph long. We seem to have collectively given up. They do state that “there are numerous challenges, including a lack of the best animal model [or any at all-Ed.], deficit corresponding to immunity, virus target in specific immune cells, and remarkable hypervariability.” (Emphasis mine.) “Remarkable hypervariability” is nothing other than a euphemism for the fact that, as Etienne de Harven has mentioned, no two identical HIV genomes have ever been found even in the same patient. The mainstream likes to blame that on wild levels of mutation, but a far more likely explanation is that these so-called “genomes” do not represent an exogenous virus at all, but are far more likely to be part of endogenous retroviral DNA that makes up 3-8% of the human genome, and which can be expressed for various reasons.

So, by the end of the article, what have we learned? It certainly reinforced the fact that in forty years, not much progress has been made. Newer and more designer style drugs have been produced, but their effectiveness remains unclear. Certainly their side effect profiles are bad enough to spur a 26,000 person class action in the U.S.

I think that the most important takeaway, though, is that the use of antiretrovirals is nowhere near as widespread as we are led to believe. Worldwide, only 70% know their status and then the rate of ARV uptake is only 2/3, leaving well more than 1/3 of a global burden of 39 million people worldwide that ought to be presenting with full blown AIDS. Where are they? The numbers, once again, do not add up, nor do they support the all too perfect HIV AIDS story the legacy media presents us with.

To support my work on Substack, please purchase my book for yourself or for a friend, and leave a review on Amazon. You can learn about efforts to ban my book here. You can also buy my new book Almost Cancelled.

If you’re a new reader and would like some background as to my views on HIV AIDS, including the “existence” question, please refer to this post and the links contained therein.