Since the earliest encounter with what was later named the SARS-CoV-2 virus (and the associated disease – and current pandemic – COVID-19), it became apparent that the disease hits different age groups differently: old individuals are the most severely affected and the group with highest COVID-19-associated death-toll.
COVID-19 victims (regardless of their chronological age) fall due to two deadly developments: acute respiratory failure and hyperproduction of proinflammatory cytokines (the “cytokine storm”). In the elderly age group, these are typically overlaid on multiple, chronic, inflammatory, aging-related diseases (ARDs), including cardiovascular disease, type-2 diabetes, and cancers. Yet even at the oldest (90+ years) cohort, we have seen spectacular (and so far not entirely explainable) cases of successful fight with the disease.
COVID-19 involves the responses from both innate and adaptive branches of the immune system, leading both to raging inflammatory process (mainly, although not exclusively, involving the lung parenchyma) and to specific reactions ending in the generation of effector lymphocytes and anti-SARS-CoV-2 antibodies. It is well known that both branches are affected by aging, and the two words that describe it are immunosenescence and inflammaging. Immunosenescence is the aging-associated decrease in the effectiveness of (mainly) adaptive immunity, while the inflammaging is a concomitant increase in paucisymptomatic secretion of proinflammatory cytokines, increasing the readiness of an elderly system for inflammatory reactivity and (although initially possible to be an adaptation) with time facilitating and fueling the ARDs.
So far it is not known what the phenotypic and/or functional characteristics of the immune system are which predispose an elderly person to develop symptomatic COVID-19 and decide (or predict) its severity or deadliness in a specific case. The immunological mechanisms underlying these variable developments upon contact of an aging individual with the virus are not known either. This Research Topic encourages detailed elucidations of both descriptive and mechanistic levels of these human/virus interactions, aiming to yield new targets facilitating curing the disease and preventing its fatal outcomes.
Since the earliest encounter with what was later named the SARS-CoV-2 virus (and the associated disease – and current pandemic – COVID-19), it became apparent that the disease hits different age groups differently: old individuals are the most severely affected and the group with highest COVID-19-associated death-toll.
COVID-19 victims (regardless of their chronological age) fall due to two deadly developments: acute respiratory failure and hyperproduction of proinflammatory cytokines (the “cytokine storm”). In the elderly age group, these are typically overlaid on multiple, chronic, inflammatory, aging-related diseases (ARDs), including cardiovascular disease, type-2 diabetes, and cancers. Yet even at the oldest (90+ years) cohort, we have seen spectacular (and so far not entirely explainable) cases of successful fight with the disease.
COVID-19 involves the responses from both innate and adaptive branches of the immune system, leading both to raging inflammatory process (mainly, although not exclusively, involving the lung parenchyma) and to specific reactions ending in the generation of effector lymphocytes and anti-SARS-CoV-2 antibodies. It is well known that both branches are affected by aging, and the two words that describe it are immunosenescence and inflammaging. Immunosenescence is the aging-associated decrease in the effectiveness of (mainly) adaptive immunity, while the inflammaging is a concomitant increase in paucisymptomatic secretion of proinflammatory cytokines, increasing the readiness of an elderly system for inflammatory reactivity and (although initially possible to be an adaptation) with time facilitating and fueling the ARDs.
So far it is not known what the phenotypic and/or functional characteristics of the immune system are which predispose an elderly person to develop symptomatic COVID-19 and decide (or predict) its severity or deadliness in a specific case. The immunological mechanisms underlying these variable developments upon contact of an aging individual with the virus are not known either. This Research Topic encourages detailed elucidations of both descriptive and mechanistic levels of these human/virus interactions, aiming to yield new targets facilitating curing the disease and preventing its fatal outcomes.