A very interesting article posted here was is the

A very interesting article posted here was is the one carried out in Asturias Spain, as if we needed further proof that Leronlimab might be beneficial in COVID, one can ask the question: if the CCR5 receptor occupancy plays a therapeutic role, can’t we expect less patients with the CCR5-Δ32 variant to be sick with COVID?

This is exactly what this study attempted. Approximately 1% of Europeans are D32-homozygotes, and carriers of this variant would be expected to have a reduced inflammatory response and hence be hospitalized with COVID

The study was based on 294 patients who required hospitalization due to COVID-19and 460 population age-matched controls. The main finding of the study was a significantly lower frequency of CCR5-D32 among the COVID-19 patients (p=0.002). But more importantly, the largest reduction (frequency) was observed in those that were severe (ICU-group) !!!

The conclusion is then that LL should work for both M/M and S/C but we could expect a good benefit on the latter group.

Obviously this study is with a reduced number of patients (294) with a population were deletion occurs in 1%, however the much less frequency of deletion encountered in the COVID patients is very telling.

Copying from the paper:

Quote:

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A polymorphism in the LZTFL1 gene located in the chemokine-receptor gene cluster (chromosome 3p) has been associated with the risk of developing COVID-19. The chemokine receptor-5 (CCR5) maps to this region, and the common 32 bp deletion variant (D32) has been associated with the extent of inflammatory disease and the outcome in several viral diseases.

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So, this yet another confirmation that our drug will very likely have a positive benefit in COVID-19. We need the numbers presto !!!!

https://www.medrxiv.org/content/10.1101/2020....20224659v1