Authors: Cuesta-Llavona E, Gomez J, Albaiceta GM, Amado-Rodriguez L, Garcia-Clemente M
PMID: 34116286 PMCID: PMC8169316 DOI: 10.1016/j.intimp.2021.107825
Abstract
The chemokine receptor CCR5 has been implicated in COVID-19. CCR5 and its ligands are overexpressed in patients. The pharmacological targeting of CCR5 would improve the COVID-19 severity. We sought to investigate the role of the CCR5-Δ32 variant (rs333) in COVID-19. The CCR5-Δ32 was genotyped in 801 patients (353 in the intensive care unit, ICU) and 660 healthy controls, and the deletion was significantly less frequent in hospitalysed COVID-19 than in healthy controls (p = 0.01, OR = 0.66, 95%CI = 0.49-0.88). Of note, we did not find homozygotes among the patients, compared to 1% of the controls. The CCR5 transcript was measured in leukocytes from 85 patients and 40 controls. We found a significantly higher expression of the CCR5 transcript among the patients, with significant difference when comparing the non-deletion carriers (controls = 35; patients = 81; p = 0.01). ICU-patients showed non-significantly higher expression than no-ICU cases. Our study points to CCR5 as a genetic marker for COVID-19. The pharmacological targeting of CCR5 should be a promising treatment for COVID-19.
Keywords: CCR5 delta32; COVID-19; Genetic susceptibility; SARS-Cov-2.
Source: https://pubmed.ncbi.nlm.nih.gov/34116286/
Archive: https://archive.is/mh3Hx
