A British lab study identifies the role played by fluvoxamine in treating COVID-19.

Key Messages

This lab study aimed to clarify the mechanism of action of fluvoxamine when used to treat COVID-19.

Genetic data from a British biobank was examined to look for any association between Sigma-1 receptor function and COVID-19 death rates.

The study confirmed that a loss of Sigma-1 receptor binding is associated with the highest death rates in COVID-19 patients. This analysis supports the theory that activation of the Sigma-1 receptor by a drug such as fluvoxamine may be responsible for the drug’s anti-COVID-19 activity.

In Vivo

Publication Date: March 3, 2021
Peer Reviewed: Yes
Publication Type: Original | Theoretical
DOI: https://www.doi.org/10.21873/invivo.12338

Homozygosity for rs17775810 Minor Allele Associated With Reduced Mortality of COVID-19 in the UK Biobank Cohort



Adult outpatients with symptomatic COVID-19 treated with fluvoxamine, compared with placebo, had a lower likelihood of clinical deterioration over 15 days. Fluvoxamine strongly binds to the sigma-1 receptor (S1R) that regulates inflammation by inhibiting the production of cytokines, believed to be responsible for severe COVID-19. We evaluated the S1R locus on chr 9p13.3 in subjects tested positive for SARS-CoV-2. We focused on SNP rs17775810 that has been previously identified by examining loss-of-function mutations in the S1R gene associated with distal hereditary motor neuropathy.

Patients and Methods:
We utilized UK Biobank (UKB) data. Data processing was performed on Minerva, a Linux mainframe with Centos 7.6, at the Icahn School of Medicine at Mount Sinai.

The effect of rs17775810 genotype on survival was significant (p=0.036, 2 tailed Fisher exact test). The minor allele homozygotes (TT) had the lowest death rate (0%), whereas the non-TT genotypes (i.e. CT and CC) had the highest death rate (16.2%).

The rs17775810 analysis corroborates the favorable effect of fluvoxamine on COVID-19 survival.