Microbial translocation, residual viremia and immune senescence in the pathogenesis of HIV-1 infection

Table 1 Main dynamics involved in the development of immune dysfunction during human immunodeficiency virus-1 infection

Microbial translocation	Residual viremia	Immune senescence
HIV-1 invasion of the gut mucosa	MT is enhanced in patients presenting residual viremia	High frequency of CD4+ CD38+ and CD8+ CD38+ T cells
Disruption of mucosal integrity and depletion of local Th-17 cells	Stochastic antigen stimulation of long-lived latency infected cells	Accumulation of senescent antigen -experienced memory T
LPS, CpG DNA in blood stream with aspecific and polyclonal immune-activation via LPS	Viral replication in anatomical sanctuaries	Inefficient T cell renewal
Pro-inflammatory cytokines secretion (TNF-α; IL-1; IL-6)	Incomplete viral suppression during cART	Fibrosis of lymphopoietic organs cells (CD28- CD57+)

HIV-1: Human immunodeficiency virus-1; Th-17: T helper-17; LPS: Lipopolysaccharide; CpG: --C--phosphate--G--; TNF-α: Tumor necrosis factor-alpha; IL-1: Interleukin-1; MT: Microbial translocation; cART: Combined antiretroviral therapy.