A recent very interesting article: https://link

A recent very interesting article:

https://link.springer.com/article/10.1186/s41231-020-00066-x

C-C chemokine receptor type 5 links COVID-19, rheumatoid arthritis, and Hydroxychloroquine: in silico analysis

This, believe it or not, shows a relation between CCR5 and HCQ (in-silico), but, more importantly, reaffirms that al the roads lead to Leronlimab !!! (CCR5/Ligands)

Quote:

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Our results showed upregulation of chemotactic factors, including CCL4, CCL8, and CCL11, that all shared CCR5 as their receptor , as a common derangement observed in both diseases; RA and COVID-19. Moreover, our results also highlighted a possible mechanism through which HCQ, which can be used as a monotherapy in mild RA or as one of the triple-DMARDs therapy (tDMARDs; methotrexate, sulphasalazine, and HCQ), might interfere with the COVID-19 infection. This might be achieved through the ability of HCQ to upregulate specific immune cell populations like activated natural killer (NK) cells, which were found to be significantly reduced in COVID-19 infection. In addition to its ability to block CCR5 rich immune cell recruitment that also was upregulated in the SARS-COV-2 infected lungs. This might explain some of the reports that showed beneficial effects.

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If this is truth, and, replicated in-vivo they propose the theory that HCQ "blocks" CCR5. This is precisely what Leronlimab does. Of course, we have proven this in-vivo already !!!!

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SARS-COV-2 infected lungs express more CCL4, CCL8, and CCL11 that share CCR5 as a common receptor

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Quote:

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In contrast, our results demonstrate a possible mechanism through which HCQ as a member of DMARDs might help in the management of COVID-19 infection, Fig (6). The possible role SARS-COV-2 infected lungs chemokines in recruiting CCR5 rich immune cells.

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We are cooking with gas my friends !!!!