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CytoDyn Inc CYDY
(Total Views: 514)
Posted On: 05/10/2020 10:15:59 PM
Post# of 153986
Posted By: thriftycents
Re: ohm20 #33258
ohm, sorry to hijack this thread but thought you might be able to answer this question that I have seen posted as your knowledge of how to interpret these medical papers seems to be immense :-)

Regarding the Kawasaki Disease symptoms seen in these children in NY, is it possible that this is related to the fact that this is a RANTES disease?

https://journals.plos.org/plosone/article?id=...ne.0011458

notes

Quote:
The CCL3L1-CCR5 axis may play an important role in KD pathogenesis. In addition to clinical and laboratory parameters, genetic markers may also predict risk of CAL and resistance to IVIG.



and

Quote:
here is evidence to suggest that recruitment of inflammatory cells in KD may be mediated through CC chemokine receptor 5 (CCR5) [15], [19], [26]. Chemotactic gradients for homing of CCR5+ cells are provided by a variety of chemokines, the most potent of which is its ligand - CC ligand 3 like 1 (CCL3L1) [27]. The genes encoding CCR5 and CCL3L1 demonstrate two distinct types of polymorphisms: single nucleotide polymorphisms in CCR5 [28] and copy number variation (CNV) in the CCL3L1-gene containing segmental duplication [29]. There is a growing interest in understanding the contribution of CNV in disease pathogenesis since it is recognized that 12% of the human genome may have undergone segmental duplications [30], [31]. We previously found that variations in CCR5 and CCL3L1 affect susceptibility to KD in parent-child trios from the United States [15].



from my elementary understanding, it seems like if what this paper is stating is true, that KD could be a potential manifestation of this being a RANTES disease and leronlimab may stop the progression of the disease to KD given that it occupies CCR5

is that a fair hypothesis?

TIA













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