The Receptor Occupancy rate and the length of RO t
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Posted On: 04/01/2021 2:17:04 PM
Re: reallypeople? #85013
The Receptor Occupancy rate and the length of RO time is very different between HIV and Covid-19.
It has to do with RANTES (CCL5).
In HIV, the virus mimics the CCL5 chemokine to gain entrance to the insides of the T-cells where it replicates. This doesn't cause the T-cells to generate all the cell signalling that can set off a Cytokine Storm. Blockade of the CCR5 receptors by leronlimab shuts down HIV and then occupies the receptors at a high rate for 60 days.
With SAR2 and the disease progression that leads to Covid-19 and a Cytokine Storm, the process is quite different.
SARS2 seeks to infect us thru the ACE2 receptors most commonly found in the lungs and gut. Our innate immune system detects the virus almost immediately and sets to work fighting it and calling for help from the rest of the immune system. It does this thru chemical signaling.
As a person's immune system is challenged, you really find out how balanced their immune system is. Do they have the right amounts of each immune component to battle the virus and clean up the debris resulting from the battle? Are there under or over expressions of receptors and cytokines before the battle?
Just how far off is the immune system from homeostasis before it is challenged? How much "energy" does the person have to fight the battle and muster the resources to renew the immune components lost and to take out the garbage?
As we know, Leronlimab's contribution to the immune response is that it controls RANTES, the chemical signalling by CCL5 that can run amok. This keeps the other immune components in better balance and prevents over and under expression of other receptors, but especially CCR5 which is so central in Covid-19 and cancer metastasis.
CCR5 is expressed on the surfaces of many immune components. As these components do battle with the virus and its consequences, many die and become debris. The body collects this debris up and eliminates it, including blockaded CCR5 receptors with leronlimab. The body then tries to generate new immune components with brand new, virgin CCR5 receptors.
This is how you get the fall in receptor occupancy rates. These new CCR5 receptors need to be blockaded with more leronlimab to continue to control RANTES. Otherwise, you have a RANTES rebound and over and under expression of receptors again - not good! The immune system is pulled further away from homeostasis again!
So, under the conditions of fighting the Cytokine Storm, CCR5 occupancy levels lasts for a much shorter time than for HIV. If the levels fall too far, you get rebound of RANTES.
It is my opinion strictly that the best dosing could be achieved with 700mgs IV initially and then 350mgs sub-q every 7 days until the Cytokine storm is over. In longhaulers too, I think every 7 days with 350mgs would keep RO topped off. Just my guess.
I am no expert in any of these matters but I do try to learn from the best. If I reflect their expertise incorrectly, I apologize and hope to be set straight.
It has to do with RANTES (CCL5).
In HIV, the virus mimics the CCL5 chemokine to gain entrance to the insides of the T-cells where it replicates. This doesn't cause the T-cells to generate all the cell signalling that can set off a Cytokine Storm. Blockade of the CCR5 receptors by leronlimab shuts down HIV and then occupies the receptors at a high rate for 60 days.
With SAR2 and the disease progression that leads to Covid-19 and a Cytokine Storm, the process is quite different.
SARS2 seeks to infect us thru the ACE2 receptors most commonly found in the lungs and gut. Our innate immune system detects the virus almost immediately and sets to work fighting it and calling for help from the rest of the immune system. It does this thru chemical signaling.
As a person's immune system is challenged, you really find out how balanced their immune system is. Do they have the right amounts of each immune component to battle the virus and clean up the debris resulting from the battle? Are there under or over expressions of receptors and cytokines before the battle?
Just how far off is the immune system from homeostasis before it is challenged? How much "energy" does the person have to fight the battle and muster the resources to renew the immune components lost and to take out the garbage?
As we know, Leronlimab's contribution to the immune response is that it controls RANTES, the chemical signalling by CCL5 that can run amok. This keeps the other immune components in better balance and prevents over and under expression of other receptors, but especially CCR5 which is so central in Covid-19 and cancer metastasis.
CCR5 is expressed on the surfaces of many immune components. As these components do battle with the virus and its consequences, many die and become debris. The body collects this debris up and eliminates it, including blockaded CCR5 receptors with leronlimab. The body then tries to generate new immune components with brand new, virgin CCR5 receptors.
This is how you get the fall in receptor occupancy rates. These new CCR5 receptors need to be blockaded with more leronlimab to continue to control RANTES. Otherwise, you have a RANTES rebound and over and under expression of receptors again - not good! The immune system is pulled further away from homeostasis again!
So, under the conditions of fighting the Cytokine Storm, CCR5 occupancy levels lasts for a much shorter time than for HIV. If the levels fall too far, you get rebound of RANTES.
It is my opinion strictly that the best dosing could be achieved with 700mgs IV initially and then 350mgs sub-q every 7 days until the Cytokine storm is over. In longhaulers too, I think every 7 days with 350mgs would keep RO topped off. Just my guess.
I am no expert in any of these matters but I do try to learn from the best. If I reflect their expertise incorrectly, I apologize and hope to be set straight.
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