Interesting article, for sure. The way I read it, however, presence of the CCR5 Delta 32 variant is positively correlated with increased susceptibility and mortality. In other words, the less people express CCR5, the more susceptible they are to COVID-19.

As misiu pointed out earlier, I think you can resolve the apparent contradiction between what we think we know about leronlimab/COVID-19 and what this article appears to say (i.e., leronlimab blocks CCR5 and appears to work in COVID, but people with less CCR5 fare worse ...) by remembering that leronlimab only partially binds to CCR5.

Presumably, this means leronlimab can modulate the runaway cascade of inflammation responsible for severe COVID-19 while still permitting the CCL5/CCR5 pathway to address the underlying disease as intended.

[EDIT: if this theory is correct, it is also important because it means maraviroc likely would be far less effective or ineffective in COVID-19, since its binding to CCR5 is far more complete]

Just my two cents from a decidedly non-scientific background.

Time will tell ...