SARS-CoV-2, COVID-19 and the aging immune system

Abstract

The coronavirus disease 2019 (COVID-19) pandemic is a global health threat with particular risk for severe disease and death in older adults and in adults with age-related metabolic and cardiovascular disease. Recent advances in the science of aging have highlighted how aging pathways control not only lifespan but also healthspan -the healthy years of life. Here, we discuss the aging immune system and its ability to respond to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We specifically focus on the intersect of severe COVID-19 and immunosenescence to highlight pathways that may be determinant for the risk of complications and death following infection with SARS-CoV-2. New or adapted therapeutics that target agingassociated pathways may be important tools to reduce the burden of death and long-term disability caused by this pandemic. Proposed interventions aimed at immunosenescence could enhance immune function not only in older adults but in susceptible younger individuals as well, ultimately improving complications of severe COVID-19 for all ages.

Seroprevalence of anti-SARS-CoV-2 antibodies 6 months into the vaccination campaign in Geneva, Switzerland, 1 June to 7 July 2021

“…The 16.2% seroprevalence of infection-induced antibodies in adults aged ≥ 75 years mirrors their previously reported lower infection risk [5,7] and the fact that they were the first age group targeted by the vaccination campaign; with a reported 92.6% vaccination rate and an associated estimated total seroprevalence of 93.1%. It is also not possible to exclude that the lower proportion of participants with infection-induced antibodies in this age group is attributable to immunosenescence or higher likelihood of antibodies waning in the elderly population [15,16].…”

Innate immune remodeling by short‐term intensive fasting

“…In our recent study, we monitored the hematological profile seven days and in some participants 14 days of intensive fasting after 7-day refeeding process, and the composition of their leukocyte's populations were more balanced after intensive fasting (Fang et al, 2021). Nevertheless, it would be helpful to examine the short-term and long-term effects of ) that challenge the effectiveness of timely developed drugs and vaccines, strengthening immunity through both medical and non-medical interventions, including but not limited to fasting, may be helpful for surviving this disease (Bartleson et al, 2021;Hannan et al, 2020). Intensive fasting causes an extreme starvation stress, which presumably triggers higher activation of autophagy than incomplete fasting does, possibly leading to a better priming of the host immune system to fight against virus diseases.…”

From online data collection to identification of disease mechanisms: The IL-1ß, IL-6 and TNF-α cytokine triad is associated with post-acute sequelae of COVID-19 in a digital research cohort

“…Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new virus causing coronavirus disease 2019 (COVID- 19) which has led to a health crisis of global scale [1,2]. COVID-19 is now recognized as a multi-organ disease with considerable mortality in risk groups [3][4][5]. With a growing population of recovering patients, it became clear that in 32-87% of patients (including those with mild acute disease) health impairments persist beyond the acute phase of infection [6][7][8][9][10].…”