This is old news for most of the audience here, but COVID-19 mortality is suffered largely by the old. An aged immune system greatly raises the odds of suffering the cytokine storm of runaway inflammation that leads to mortality. One of the characteristics of an aged immune system is a heightened level of chronic inflammatory signaling, a reaction to the damaged environment of aged tissue. As researcher here note, the presence of age-related chronic inflammation creates a vulnerability to the risk of much greater, excessive and unrestrained inflammation in response to infection.
Aging is characterized by the dynamic remodeling of the immune system designated "immunosenescence," and is associated with altered hematopoiesis, thymic involution, and lifelong immune stimulation by multitudinous chronic stressors, including the cytomegalovirus (CMV). Such alterations may contribute to a lowered proportion of naïve T-cells and to reduced diversity of the T-cell repertoire. In the peripheral circulation, a shift occurs towards accumulations of T-cell and B-cell populations with memory phenotypes, and to accumulation of putatively senescent and exhausted immune cells.
The aging-related accumulations of functionally exhausted memory T lymphocytes, commonly secreting pro-inflammatory cytokines, together with mediators and factors of the innate immune system, are considered to contribute to the low-grade inflammation (inflammaging) often observed in elderly people. These senescent immune cells not only secrete inflammatory mediators, but are also able to negatively modulate their environments. In this review, we give a short summary of the ways that immunosenescence, inflammaging, and CMV infection may cause insufficient immune responses, contribute to the establishment of the hyperinflammatory syndrome and impact the severity of the coronavirus disease 2019 (COVID-19) in elderly people.