Conversely, PBMCs from progressor macaques presented an upregulation of CD4, as well as of CD59, which inhibits complement-mediated cell lysis to protect cells from complement damage, and CD101, which has been proposed as a marker of pathological responses to dysbiosis; they also presented a downregulation of IFNL1, which plays a role in viral and bacterial infections, as well as the proinflammatory cytokine gene IL1B. This evidence concerns the gene CD59 and bacterial infectious disease.