MAGT1, a magnesium transporter gene, was recently discovered to be associated with X-linked human T-cell immunodeficiency. Free Mg2+ acts as an intracellular second messenger that affects the activation of phospholipase Cγ1, and the balance of Ca2+ in the T-cells. A MAGT1 deficiency prevents an influx of Mg2+, and consequently hampers signaling in the T-cells, reducing their effectiveness.
Two sub-group populations were used to sequence the MAGT1 gene via Sanger sequencing and linkage disequilibrium. Once sequenced, the polymorphisms in HIV+ patients were compared with polymorphisms in a control (non-HIV affected) group of patients. Given that reduced expression of MAGT1 impedes T-cell processes and therefore limits the immune system's efficiency, MAGT1 may be connected to the contraction or development of HIV in a patient.