The next Berlin Patient

What was the very first AIDS 2024 Presentation Chosen by the Co-Chair? The next Berlin Patient.

So, they are saying that the Latest HIV Cure Case Is the Most Encouraging One Yet. Let's say they are close. But the LATCH study shall exceed even this accomplishment.

Why is it so Encouraging?

"Unlike previous cases, however, the patient was cured without needing donated stem cells from someone genetically immune to HIV."

...

"Brown and most others like him in the years since have received bone marrow from donors with two copies of a particular mutation in their CCR5 gene, which regulates the CCR5 receptor found on white blood cells. The mutation, called CCR5-delta 32, makes immune cells naturally resistant to infection from strains of HIV-1 (the more common type of HIV). By transplanting stem cells containing the mutation to HIV patients, the hope is that you can transfer over that resistance as well, allowing their bodies to permanently eliminate the virus*.*

Just a small percentage of people carry two copies of the CCR5-delta 32 mutation*, however, and Charité doctors were only able to find a compatible* donor for their patient who carried one copy*. But to everyone’s surprise, the switch* still worked*. The patient chose to* stop taking his HIV medication in 2018 and tests have continued to show no traces of the virus in his system (he also remains cancer-free). The man is now believed to be the seventh person cured of HIV using stem cells*, but the first* without needing both copies of the CCR5-delta 32 mutation*."*

An estimated 15,000 individuals were at the 2024 AIDS conference. Were any made aware of LATCH? Doubt it.

What did Dr. Lalezari say about LATCH?

"Dr. Lalezari 16:29: LATCH, Stem Cell Transplant HIV Cure

In addition to these two core clinical studies, I'm pleased to announce two other exciting clinical initiatives. First, we are in discussion with the American foundation for AIDS research to partner and co-sponsor a study called LATCH, led by investigators at Oregon Health Sciences University and the University of Washington, LATCH stands for Leronlimab and Allogeneic stem cell Transplant to Cure HIV*.*

The proposed study will evaluate the use of leronlimab to facilitate an HIV Cure in the HIV positive subjects, undergoing stem cell transplantation. Previous reports of HIV Positive patients achieving a cure have occurred when those RARE homozygous CCR5, double negative individuals have been identified to provide donor stem cells for the transplantation.

This study will evaluate the possibility that leronlimab could extend the list of potential donors to include the much larger pool of CCR5 positive individuals*. Leronlimab would be administered following transplantation for six months during the engraftment period, to* protect the HIV negative, donor cells from becoming HIV infected. The hope is that those donor cells now protected from HIV infection, will then eliminate HIV from the reservoir of the transplant recipient*. If successful, this study would obviously bring about much needed positive attention to both leronlimab and CytoDyn. We're exploring* this partnership with AMFAR to jointly co-sponsor and fund the research aspects of the LATCH study, which importantly, will not require us to cover the cost of the transplant itself*."*

Did you catch that? The Stem Cell donor pool can be ANYBODY with Sterile Stem Cells in LATCH. Unlike the next Berlin Patient, where the Stem Cell Donor had just (1) copy of the CCR5-delta 32 mutation, in LATCH, the Stem Cell donors shall have no CCR5-delta 32 mutations. This certainly exceeds the "most encouraging one yet" because the cure of HIV utilizing Stem Cell Transplantation would be attributed to leronlimab and not to the need for the mutation to exist in the Stem Cell Donor.

"At this point, it’s not clear exactly how the next Berlin Patient was able to clear his HIV completely. People with only one copy of the CCR5-delta 32 mutation can still get infected by HIV*, though it does seem to reduce the odds of catching it. So, it’s possible that even one copy is enough to help eliminate its presence in someone already infected. But it’s also possible that* simply flushing away an HIV-infected person’s immune system and replacing it with a new one, regardless of whether the CCR5-delta 32 mutation is around, can do the same. That said, other HIV patients who have received stem cell transplants from non-CCR5-delta 32 donors have seen their infections rebound within months*, so other factors might be important to a cure, such as how quickly the donated immune system takes over."*

In my opinion, the next Berlin patient, in addition to receiving a Stem Cell Transplant which included CCR5-Delta 32 mutation, leronlimab was also administered in a fashion similar to how it shall be administered in the LATCH study.

"Leronlimab would be administered following transplantation for six months during the engraftment period, to protect the HIV negative, donor cells from becoming HIV infected. The hope is that those donor cells now protected from HIV infection, will then eliminate HIV from the reservoir of the transplant recipient*.*"

If leronlimab were not administered, how then would those Stem Cell Donor Cells not become infected with HIV, since HIV would be permitted to enter the CD4-T cell.

HIV CD4 Cell Entry Blockade by Leronlimab

So, at the AIDS conference, they discussed the 7th instance of a patient achieving an HIV cure. But did not get into all the details of how that happened. Only discussed the fact that there was only one copy of the CCR5-Delta 32 mutation in the gene population of the Stem Cells administered for the transplant. But there was no mention that the same could have been achieved without any of the Donor Stem Cells containing the same mutation, which is exactly the proposition of the LATCH study that shall be conducted early 2025.

Furthermore, there was no mention of any drug that was administered in conjunction with the Stem Cell Transplant to the next Berlin Patient, but it is clear, that something had to protect the only half-way guarded Stem Cells from HIV invasion. Some HIV could enter the cell because CCR5 still existed to some degree. Certainly, that degree was reduced significantly, due to there only being one mutation copy, but HIV would still find a way to enter the cell. And if HIV could enter the cell, then there would be replication even if HAART was also administered. HAART would also have a tendency to drive HIV deeper into the Reservoirs.

So then, there shall be HIV cures with Stem Cell Transplant in any of 3 types of HIV Sterile Donors. Stem Cells with 2 copies of CCR5-delta 32 mutation, Stem Cells with only 1 copy of CCR5-delta 32 mutation and Stem Cells with 0 copies of CCR5-delta 32 mutation. Leronlimab makes this a moot point. In order to achieve HIV Cure using Stem Cell donors, the only medication that is required to make this happen is leronlimab. No other medication can do it because no other HAART prevents HIV from entering the CD4 T Cell via 100% blockade of CCR5. HAART works within the cell as per the graphic above. Leronlimab works outside the CD4 - T Cell, on the CCR5 receptor thereby preventing HIV from entering and therefore prevents HIV replication.

What will happen when it is proclaimed to these same 15k individuals that leronlimab led to the curing of the 8th patient of HIV and that patient had 0 CCR5-delta 32 mutations? That is the aim of the LATCH study, to accomplish this exact HIV cure many times over. Not just 8, but 28 or more. Why was leronlimab not mentioned? Do they believe we are so foolish to believe that HAART protected the sterile HIV Stem Cells from being infected? How could they? They still allow HIV to enter the cell and therefore, despite HAART administration, there would still be some replication which would permit HIV to be distributed back into the reservoirs, (which is NOT a cure). Do they think we should believe that no medication was co-administered? Then what prevented HIV from entering even the cell. Yes, there was some effective CCR5 receptors present, even with only one CCR5-delta 32 mutation. Still some functional CCR5 existed, so therefore, HIV could enter the CD4-T cell and replicate. If that was still a possibility, and if no medication was co-administered to protect the healthy, non-infected CD4 - T Cells, then why did they not get infected by HIV? They HAD to be protected, but that protection was not mentioned. Why not?

You mean, they left it out, to protect their narrative? Protection of their silly, ignorant narrative. But, come the LATCH study, leronlimab is part of the acronym. Sudden destruction about to be fulfilled. An Extraordinary day is coming.

Scott Hansen relates in the 5/30/24 Webcast:

"Scott Hansen 23:41: 17 variants of leronlimab

First and I think Jay concluded his first section of his talk on this is to protect and expand our IP portfolio. We are working with a local generative AI company to design and create not only a longer lasting leronlimab, but possibly a more potent molecule that can be used in pre-exposure prophylaxis or PREP. A space where we think in combination with a long-acting antiretroviral, will have huge impacts for the HIV community.

I'm currently testing 17 new variants of leronlimab. It's really early in this process, but some of these new molecules are showing extreme promise in my in-vitro assays. I'm making sure that the function of leronlimab is not altered, but preserved, and these data are very exciting and yet very, very early, but very promising.

I'm very excited about this endeavor and I feel it will be a game changer for CytoDyn and will help preserve the company's future. Lastly, I feel another game changer for CytoDyn, is the LATCH trial Jay mentioned earlier in his presentation. This is something very exciting for us as a company and me, personally, I became a scientist, not only to move science forward, but to also to try to save life, Dr. Jonah Sasha's work with leronlimab and stem cell transplant in the non-human primate model really made this trial possible for us. He demonstrated that you can pharmacologically knock out CCR5 with leronlimab, essentially creating that Delta 32 phenotype that Jay mentioned. The phenotype has facilitated HIV CURE in the setting of stem cell transplantation.

Obviously, this isn't a therapy for everyone living with HIV, but for those that it makes sense for, we believe leronlimab can help cure people of HIV and that would be pretty remarkable and something we can all be very proud of. I can go on and on about my excitement about this molecule, but for the sake of time, I'm going to hand the mic back over to Jay."

Is it any wonder then, that Dr. Sasha was moved to the top of the Scientific Board of Expert Advisors? For a refresher of what he has been up to, consider My69z's repost of a long time favorite of mine.