I’m going to briefly react to the following article, published in Nature Reviews Immunology in 2021, written by Barton F Haynes. I’m sure I’m not the only one that is giving the side eye to the fact that a (actually multiple) “vaccine(s)” for Covid were produced in under a year; yet after 39 years of effort, there remains no vaccine for the wily “HIV.”
SARS-CoV-2 and HIV-1 — a tale of two vaccines
Here’s the pull quote:
The rapid development of COVID-19 vaccines and their deployment in less than a year is a scientific and medical triumph that has raised a key question. Why do we have several SARS-CoV-2 vaccines but do not have a single HIV-1 vaccine?
Excellent question—let’s see how the authors explain this dramatic failure of the HIV AIDS paradigm. Jumping in (emphasis mine throughout):
In December 2019, the WHO was notified of a cluster of viral pneumonia of unknown origin, and the first draft genome of the causative virus, SARS-CoV-2, was published in January 2020. By the end of 2020, several SARS-CoV-2 vaccines had been developed. Two of these were shown to be ~95% effective in preventing symptomatic COVID-19 in phase III efficacy trials and received approval by the FDA for deployment under Emergency Use Authorization before the end of the year. By contrast, four decades ago, in the summer of 1981, the first individuals with what would be known as acquired immunodeficiency syndrome (AIDS) were described, and, in 1983, the aetiological agent of AIDS, HIV-1, was isolated — yet, we still do not have a globally protective HIV-1 vaccine.
I have a suspicion that in the next few years, perhaps as a kind of reaction against the ascendancy of RFKJ and the growing acceptance of alternatives to pharma-driven mainstream medicine, there is going to be a huge push to develop an mRNA vaccine for “HIV.” Whether this game is a wise one for the HIV AIDS establishment to play remains to be seen; however, the following X post by @JacquiDeevoy1 indicates that I am not the only person who might be thinking this way, or at least wonder about some recent developments in “HIV” testing (h/t Celia Farber):
If you read the comments to this post, you will see that many people have been noticing the accelerated push for “HIV” testing that’s happening, seemingly, all of a sudden—why? Here’s the link to Celia’s piece about Mr. Starmer publicly taking an “HIV” test. Now, back to the article. As far as I’m able to discern, the official reason it is so hard to make an “HIV” vaccine is multifaceted, but largely has to do with its incredible variability—so variable, in fact, that no two identical “HIV” genetic sequences have ever been found even in the same patient, but of course this article leaves that out. The authors may not even be aware of that particular tidbit.
For HIV-1, two general strategies have been tested in vaccine efficacy trials: the induction of CD8+ T cells that kill HIV-1-infected cells, and the induction of non-neutralizing antibodies that protect from HIV-1 transmission by Fc receptor-γ (FcRγ)-mediated antiviral effector functions. Like SARS-CoV-2-neutralizing antibodies, HIV-1 non-neutralizing antibodies are easily induced by any of a number of HIV-1 Env monomers or open trimers. However, out of seven HIV-1 vaccine efficacy trials carried out to date, six have failed. The seventh, called RV144, which was carried out in Thailand by the US Army, showed minimal protection of ~31%, and non-neutralizing antibodies with FcRγ-mediated antiviral effector functions served as correlates of decreased transmission risk7.
Go back and read that highlighted section again. What does that tell you?
Nonetheless, the ultimate aim of HIV-1 vaccine development is induction of broadly neutralizing antibodies (bnAbs)8. Whereas SARS-CoV-2-neutralizing antibodies are easily induced within ~10 days of onset of COVID-19 symptoms and within 2 weeks of vaccination, HIV-1 bnAbs are not readily induced by vaccination, nor in infection, and only occur at very high levels in ~10% of individuals infected with HIV-1 after years of infection. Roadblocks for the induction of HIV-1 bnAbs are the presence of a dense and poorly immunogenic Env glycan shield, molecular mimicry of Env epitopes that induce cross-reaction of antibodies with human proteins, and variable loop regions in Env that can induce competing non-protective antibodies. Most importantly, HIV-1 bnAbs have unusual traits such as autoreactivity, long third heavy chain complementary determining regions (HCDR3s) and are enriched in rare somatic mutations — all of which make bnAb precursors either very rare owing to immune tolerance deletion or difficult to activate9,10.
The rest of this article discusses the strategy, which seems to be in vogue now, of targeting B cells to produce these antibodies. It’s unclear to me how this is going to prevent infection with “HIV,” given that to be “HIV” antibody positive means that the patient has already produced antibodies. How many antibody responses do we really need for one alleged virus? If anyone reads this article and sees something I don’t, please comment below. To me, this sounds like more wild backpedaling and frantic explanations as to why we will never have an effective vaccine for “HIV;” and possibly not a safe one, either. To conclude:
The significance of successful germline-targeting and sequential HIV-1 immunogen design goes beyond making the long-awaited HIV-1 vaccine. Learning the rules for safely guiding bnAb B cell lineages should improve the development of other difficult-to-make vaccines, and also hold lessons with regard to avoiding undesired immune responses such as the development of pathogenic autoantibodies.
Oh look, they’re already hedging their bets. We may never be able to produce an “HIV” vaccine but our quest to develop one might help us develop other vaccines, for other diseases, forever! Lord help us all.
It is interesting that 'HIV' being a 'quasi-species', because of its wild variability and mutation rate, yet the same antigens and primers are used year after year for 'it'. Nutty.
Since they are all fraudulent products, maybe the AIDS thing was just a trial run for what would become a worldwide campaign (COVID). It's a huge data collection event first and foremost.