Innate DNA sensing is impaired in HIV patients and IFI16 expression correlates with chronic immune activation

• DOI: 10.1111/cei.12317
• Publication Date: 2014-03-05T10:08:45Z
• Authors: S K Nissen; J F Højen; K L D Andersen; E Kofod-Olsen; R K Berg; S R Paludan; L Østergaard; M R Jakobsen; M Tolstrup; T H Mogensen
• Keywords: Adult; CD4-Positive T-Lymphocytes; Male; 0303 health sciences; Intracellular Space; HIV; Nuclear Proteins; HIV Infections; DNA; Middle Aged; Lymphocyte Activation; Phosphoproteins; ADP-ribosyl Cyclase 1; Nucleotidyltransferases; Immunity, Innate; 3. Good health; 03 medical and health sciences; Receptors, Pattern Recognition; Chronic Disease; Humans; Female; Immunologic Memory; Cells, Cultured

The innate immune system has been recognized to play a role in the pathogenesis of HIV infection, both by stimulating protective activities and through contribution chronic activation, development immunodeficiency progression AIDS. A for DNA sensors recognition suggested recently, aim present study was describe influence infection on expression function intracellular sensing. Here we demonstrate impaired interferon-stimulated genes responses peripheral blood monuclear cells from HIV-positive individuals, irrespective whether patients receive anti-retroviral treatment. Furthermore, show that levels interferon-inducible protein 16 (IFI16) cyclic guanosine monophosphate-adenosine monophosphate synthase were increased treatment-naive patients, IFI16 correlated with high viral load low CD4 cell count. Finally, our data correlation between CD38 expression, marker CD4(+) central effector memory T cells, which may indicate IFI16-mediated sensing signalling contributes activation. Altogether, demonstrates abnormal cytosolic have implications control opportunistic infections, activation death.