Well, I guess I can answer my own question and tha

Well, I guess I can answer my own question and that's is our current sub-cutaneous approach reaches a functional cure, but I believe they are seeking an outright TOTAL cure by their statement:

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there is an urgent need to design a functional cure via elimination of the viral reservoir.

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If you eliminate the viral reservoir and you drive viral load to zero, you have effected a Total Cure.

They also say a functional cure is devoid of CCR5:

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While a CCR5-deficient immune system can demonstrably yield a functional HIV cure,

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In fact, this is a Total Cure.

Since what you state here is correct:

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Leronlimab already acts as a functional cure in quite a large percentage of patients. In combo therapy with leronlimab 81% of patients were less than 50 c/ml which I believe was 350mg. In monotherapy I believe it was 91% or 92% of patients that were under 50 c/ml at 700mg.

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Why are they spending the $1million annually to get this achieved? It is because they want what you have said PLUS they want to eradicate the reservoir which our current solution does not do.

The proposed solution is to:

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Deliver these therapeutics to the relevant immune cell type. In specific aim 1, we will generate and characterize AAV bearing capsids that target T and B cells specifically across both macaques and humans. In aim 2, we will demonstrate proof-of-concept utility of these new AAVs by delivering Leronlimab to SHIV-infected, ART suppressed macaques to determine if a functional cure can be achieved with this approach. This work would expand our knowledge of the mechanism of HIV cure by showing the utility of long-term antibody-based competitive CCR5 inhibition and establish a new set of AAV vectors to support in vivo delivery of anti-HIV therapeutics.

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Certainly, they believe the Reservoir of HIV resides in the T and B cells. But what if HIV is in the NKCs, the Macrophages, the Dendrites, the monophils, eosinophils, basophills. What if they are in the platelets? What if they are in the brain or in the GI tract cells?

And what are these capsids to do? Infect the targeted T and B cells. Then what? Release Leronlimab? What good would that do? For HIV, LL acts as entry inhibitor. Entry into CD4 T lymphocytes. When these capsids enter the T and B cells, and if they find dormant HIV there, releasing LL won't stimulate them to action. If the viral capsid causes the T and B cells to lyse and open thereby releasing both the LL and the dormant HIV, then I would understand that LL would have greater affinity to the CCR5 receptor and bind instead of the dormant now active HIV.

But what is the plan, to cause all the B cells and T cells to lyse?
I have to read about this some more, but if anyone could enlighten me...