Study in Nature Biotechnology came

Study in Nature Biotechnology came out on June 26, 2020 from researchers in Germany, independent of CytoDyn that supports Dr. Patterson's CCR5 blocking theory in quelling COVID-19. (Why this research has not made headline news on the Leronlimab boards or I missed it is surprising.) The researchers Robert Lorenz Chua, Soeren Lukassen, Saskia Trump, Bianca P. Hennig, and Daniel Wendisch, corroborate Dr. Bruce Patterson's theory that blocking CCR5 may is one of two chemokine receptors that likely can treat the cytokine storm due to Covid-19 in severe to critical patients. Based on these converging findings, it appears that Leronlimab is poised to make a dramatic statement with its treatment results very soon, since it is the only safe drug to target the CCR5 receptor in the treatment pipeline. This finding increases the odds that Leronlimab could very well be the CV wonder drug many have been hoping for, and moreover change the trajectory of this pandemic. Lastly, seeing Dr. Patterson's work partially replicated by an independent group nearly ensures that his paper will finally get published... (rumored to be in the same journal). Dr. Patterson could very well be hailed as the scientist who made the major research breakthrough the world needed to overcome this deadly disease.

"Our data suggest the possibility of targeting chemokine receptors. We found a significant induction of CCL2 and CCL3 expression in macrophages together with an increased expression of CCR1, the receptor for both chemokines, in patients with critical COVID-19. Because binding of CCL2 or CCL3 to CCR1, CCR2 or CCR5 can induce monocyte recruitment into the lung parenchyma with subsequent differentiation into inflammatory macrophages and consecutive recruitment and activation of additional immune cells and epithelial damage, CCR1, CCR2 and CCR5 might represent promising anti-inflammatory targets in COVID-19. Targeting the CCR2/CCL2 axis has been introduced in HIV and other viral infections53. However, we did not observe CCR2 expression in the respiratory tract of patients with COVID-19 (presumably because of its rapid downregulation in monocytes as they exit the bloodstream and enter tissues; Extended Data Fig. 7), leaving CCR1 and/or CCR5 as potential therapeutic targets."

Here is the source... https://www.nature.com/articles/s41587-020-0602-4

Please thank poster THNT on SA for making us aware of this study that apparently slipped past everyone else's radar.

Very encouraging indeed!

OU