full article here:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4174864/
"Although numerous infections are successfully cleared by the acute immune response, certain viral infections are not resolved and result in chronicity. The function of virus-specific T cells during chronic infections is often characterized by varying degrees of impairment, leading to defects in the ability of the host to eliminate the pathogen. Depending on the antigenic load generated by the infectious agent the impaired memory formation can result in T cells becoming either senescent or exhausted (
9). Thus, immune senescence arises as a consequence of low-grade antigenic stimulation with the resulting inflammation determining the rate of senescence, as seen with CMV or EBV infection and not age
per se (
10,
11). The quantity of the lifelong antigenic load and the resulting inflammation determines the rate of immune senescence. Whereas a high-antigen load, caused by HIV, HCV, and HBV infection, leads to the formation of exhausted T cells (
12)"
"Senescence manifests itself in T cells as the loss of the co-stimulatory molecule CD28 and the acquisition of innate markers such as killer-cell lectin-like receptor G1 (KLRG-1), while senescent T cells lose proliferative capacity they retain their cytotoxic activity and secretion of TNFα and IFNγ (
17–
19)."
"Senescent human CD8+ T cells isolated from healthy donors stimulated through the TCR have been shown to preferentially utilize glycolysis and also exhibit mitochondrial dysfunction and impaired mitochondrial biogenesis, which may explain their dependence on glycolysis for energy (
17). The ability of a T cell to undergo mitochondrial biogenesis leads to an increased capacity of the cell to respond to metabolic stress, a characteristic termed spare respiratory capacity (
2). It has been demonstrated that, unlike other memory subsets senescent CD8+ T cells have a substantially reduced spare respiratory capacity making them energetically unstable (
17)."