The first longhauler's index diagnostic paper repo
Post# of 148165
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Posted On: 06/30/2021 2:24:52 PM
The first longhauler's index diagnostic paper reporting low CCL4 was out in pre-print in December, and recently published. It's good to see the latest pre-print regarding the theory behind long-hauler's, and the finding that non-classical monocytes may accumulate (intermediate state monocytes do not migrate out of blood stream due to low CCL4, and persist a long time for some other unmentioned reasons only alluded to in Dr. Been interview last week), continue presenting S1 spike protein, interact with endothelial cells, and cause havoc in general.
I don't follow the argument that:
"The use of Leronlimab would produce a reduction of the CCL4-mediated recruitment of activated T-cells (proposed as an alleviation to PASC.)" If it's low CCL4-mediated recruitment of intermediate monocytes out of the bloodstream causing long-hauler's (via persistence then differentiation into non-classical monocytes), how would reducing that recruitment further help PASC?
BP mentioned in his recent Been interview something about exercise increases mobilization of monocytes (see ref from paper https://pubmed.ncbi.nlm.nih.gov/29957728/) and that LL may help prevent this.
But it isn't clear why reducing monocyte migration would be good for PASC if it's that reduced migration out of the blood that causes the propsed pathogenesis of PASC to begin.
The paper isn't clear about the issue either:
The bolded part makes no sense / is not a complete sentence.
Can anyone help me out here? I thought low migration of intermediate monocytes was the proposed cause of PASC, so why would reducing the migration further with LL help the condition?
I don't follow the argument that:
"The use of Leronlimab would produce a reduction of the CCL4-mediated recruitment of activated T-cells (proposed as an alleviation to PASC.)" If it's low CCL4-mediated recruitment of intermediate monocytes out of the bloodstream causing long-hauler's (via persistence then differentiation into non-classical monocytes), how would reducing that recruitment further help PASC?
BP mentioned in his recent Been interview something about exercise increases mobilization of monocytes (see ref from paper https://pubmed.ncbi.nlm.nih.gov/29957728/) and that LL may help prevent this.
But it isn't clear why reducing monocyte migration would be good for PASC if it's that reduced migration out of the blood that causes the propsed pathogenesis of PASC to begin.
The paper isn't clear about the issue either:
Quote:
In summary, the mechanism of PASC discussed in this report suggests that intermediate monocytes remain in circulation due to low CCL4 levels extending their time to differentiate leading to an accumulation of non-classical monocytes. The utility of using CCR5 antagonists in preventing migration of intermediate and non-classical monocytes due to the elevated levels of CCL5/RANTES in PASC5.
The bolded part makes no sense / is not a complete sentence.
Can anyone help me out here? I thought low migration of intermediate monocytes was the proposed cause of PASC, so why would reducing the migration further with LL help the condition?
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