Leronlimab Treatment Inhibits CCR5 in Critically Ill COVID-19 Patients–Decreasing Inflammatory Cytokines, Increasing CD8 T-Cells, and Decreasing SARS-CoV-2 RNA in Plasma by Day 14

Researchers have reported that treatment of ten critically ill COVID-19 patients with the anti-CCR5 monoclonal antibody leronlimab restored depressed CD8 counts which correlated inversely with decreases in plasma viral load of SARS-CoV-2, which moved to undectable by Day 14 of treatment, and that 6 of 10 treated patients showed significant improvement during the 14-day test period. The scientists noted that levels of the normal CCR5-binding immunomodulatory molecule CCL5/RANTES is elevated 3- to 5-fold in mild to moderate COVID patients and over 1000-fold in critical COVID patients, suggesting that blocking the binding of this immunomodulatory molecule might have an influence in COVID-19. The newly reported results include the first report of the highly sensitive measurement of quantitative plasma viral load by droplet digital PCR (ddPCR) in COVID patients. The researchers also described a statistically significant drop in interleukin-6 (IL-6) by Day 14 of leronlimab treatment. In addition, single-cell transcriptome analysis revealed decreased in IL-6 in myeloid cells. The work was reported online on November 9, 2020, in the International Journal of Infectious Diseases. The open-access article is titled “CCR5 Inhibition in Critical COVID-19 Patients Decreases Inflammatory Cytokines, Increases CD8 T-Cells, and Decreases SARS-CoV2 RNA in Plasma by Day 14” (https://www.ijidonline.com/article/S1201-9712(20)32305-5/fulltext). The authors conclude that, while the current study design precludes clinical efficacy inferences, the results implicate CCR5 as a therapeutic target for COVID-19 and form the basis for ongoing randomized clinical trials. Leronlimab is produced by CytoDyn, Inc., a Vancouver, Washington-based, late-stage biotechnology company (https://www.cytodyn.com/).
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