No abstract

Immunosenescence is marked by a systemic process named inflammaging along with a series of defects in the immunological activity that results in poor responses to infectious agents and to vaccination. Inflammaging, a state of low-grade chronic inflammation, usually leads to chronic inflammatory diseases and frailty in the elderly. However, some elderly escape from frailty and reach advanced age free of the consequences of inflammaging. This process has been called immunological remodeling, and it is the hallmark of healthy aging as described in the studies of centenarians in Italy. The biological markers of healthy aging are still a matter of debate, and the studies on the topic have focused on inflammatory versus remodeling processes and molecules. The sub-clinical inflammatory status associated with aging might be a deleterious event for populations living in countries where chronic infectious diseases are not prevalent. Nevertheless, in other parts of the world where they are, two possibilities may occur. Inflammatory responses may have a protective effect against these infectious agents. At the same time, the long-term consequences of protective immune responses during chronic infections may result in accelerated immunosenescence in these individuals. Therefore, the biological markers of healthy aging can vary according to environmental, cultural, and geographical settings that reflect worldwide, and in a non-biased, non-westernized perspective, the changes that we experience regarding our contacts with microorganisms and the outcomes of such contacts.

No abstract

Risk factors for the development of severe COVID 19 include several comorbidities, but age was the most striking one since elderly people were disproportionately affected by SARS Cov 2 Major drivers that can explain this markedly unfavourable response in the elderly are inflammaging and immunosenescence Recent reports have shown that the relationship between immunosenescence and COVID 19 can be bidirectional, since hospitalized patients with severe COVID 19 have an accumulation of senescent T cells suggesting that immunosenescence can be also exacerbated by SARSC oV 2 infection Therefore, the present work was designed to examine the emergence of immunosenescence in a longitudinal study in two distinct cohorts of COVID 19 patients, and to determine whether the senescence alterations were restricted to severe cases of the disease Our data, with patients from Portugal and Brazil, identified their distinctive inflammatory profile and provided evidence of increased frequencies of senescent and exhausted T cells within a seven day period in patients with mild to severe COVID 19 These results support the view that SARS CoV 2 infection can accelerate immunosenescence in both CD4 and CD8 T cell compartments in a short period of time Key words COVID 19, immunosenescence, T cell exhaustion, T cell senescence, inflammatory cytokines, inflammaging