HIV infection confers distinct mechanisms in severe drug eruption: Endogenous virus activation with aberrant Th2/Th1 and CD8 T cells function.

Severe drug eruption (SDE), a common skin disease, becomes dangerous when it occurs in patients with human immunodeficiency virus (HIV). However, the molecular mechanisms are poorly understood. Forty patients including HIV SDE (n = 15), HIV SDE (n = 15) and HIV SDE (n = 10) subjects were enrolled in our study. All HIV patients were at acquired immune deficiency syndrome (AIDS) stage. Serum levels of TNF-α, IFN-γ, IL-4, IL-13, IL-6, CXCL9, and CCL17 were quantified by ELISA. Epstein-Barr virus (EBV) and cytomegalovirus (CMV) loads were quantified by RT-qPCR. CD4, CD8, Th1, Th2, TNF-α-CD8, and IFN-γ-CD8 T cell populations were measured by flow cytometry. Levels of biochemical indexes in HIV SDE patients were significantly different from in HIV SDE patients (P < .05). EBV and CMV viral loads were significantly higher in HIV SDE patients, but not in HIV SDE patients (P < .05). Inflammatory cytokines TNF-α and IFN-γ were significantly elevated in HIV SDE patients (P < .05). Th2/Th1 populations and TNF-α secreting or IFN-γ secreting CD8 T cells, were significantly up-regulated in HIV SDE patients compared to HIV SDE patients (P < .05). Conversely, the CD4/CD8 ratio was significantly down-regulated in HIV SDE patients compared to HIV SDE patients (P < .05). HIV infection confers distinct clinical phenotypes and immune inflammatory mechanisms in SDE. Sustained EBV and CMV activation, unbalanced Th2/Th1 and overactive CD8 T cells mediating a pro-inflammatory response could act as distinct mechanisms in the aggravation of SDE in HIV SDE patients.