Mutations in the GLS2 gene facilitate severe Staphylococcus aureus bacteremia (SAB)
Complicated course of Staphylococcus aureus bacteremia is associated with GLS2 mutations, as shows study on 240 patients.
S. aureus bacteremia (SAB) is a disease of skin which may infect bloodstream, joints, bones and even heart. Its incidence ranges from 10 to 30 per 100,000 individuals. Although falling for SAB is a consequence of complex factors (including quality of health care), the further fate of a patient is partially influenced by genetics.
Gene GLS2 manages part of glutamine metabolism, which is vital for immune system cells. Mutations resulting in lower activity of the gene or an improper product of the gene were found to be a significant factor in 206 patients with severe SAB, in contrast to 204 uncomplicated cases. Additionally, an activity of the gene was measured in healthy people and mice models to prove the causal role of GLS2. Experimental deactivation decreased the activity of one of the interleukin genes, which play an essential role in the immune response.
Across nearly 11 thousand variants, the most severe of identified were: rs2657878 and rs2657879.
The study points to the potentially beneficial sequencing of a single gene to predict possible progression of Staphylococcus aureus bacteremia.
More: “Human genetic variation in GLS2 is associated with development of complicated Staphylococcus aureus bacteremia”, W. Scott et al., 2018, doi:10.1371/journal.pgen.1007667.