COVID-19, Virology and Geroscience: A Perspective

Abstract

Until 2002, coronaviruses (HCoV-NL63, HCoV-229E, HCoV-OC43 and HKU) were first known to cause common cold in humans. However, in 2002 the SARS-CoV emerged, and then in 2013 the MERS-CoV. The SARS-CoV and MERS-CoV caused severe respiratory syndrome and were highly pathogenic for humans, because of their ability to adapt to their host, notably to increase affinity for their receptor, leading to high infectivity in humans (1, 2). In December 2019, a new coronavirus, first called 2019-nCov and then SARS-CoV-2 for severe acute respiratory syndrome coronavirus 2, was identified in Wuhan, China (3). SARS-CoV-2 spreads very efficiently, causing the current COVID-19 (Coronavirus Disease 2019) pandemic, that by mid-May 2020 has already killed more than 300,000 people all over the world. The highest morbi-mortality of COVID-19 is observed among older patients (4). Patients in intensive care unit (ICU) are older than patients not requiring ICU (5). In a study using an observational database from 169 hospitals in Asia, Europe, and North America, an age of more than 65 years-old was associated with a higher risk of in-hospital death: 10.0% mortality rates for people ≥ 65 years-old vs. 4.9% for those < 65 years-old (6). In France, 3.6% of infected individuals needed to be hospitalized, with an average death rate of 0.7% ranging from 0.001% in individuals < 20 years-old, to 10.1% in those > 80 years-old (7). Not all older adults appear to be equally vulnerable to SARS-CoV-2 infection (8). Frailty is a clinical syndrome in older adults characterized by an increased vulnerability for adverse health outcomes and aging-associated functional declines (9). Frail older adults, especially those with comorbidities (eg, hypertension, obesity, diabetes) are at higher risk of death if they get infected than younger adults (10). Prevention interventions need to be developed to reduce the impact of COVID-19 in older people. Geroscience is an interdisciplinary field that seeks to understand the links of biological mechanisms of aging with biological mechanisms of disease and body functions (eg, mobility, cognition) to ultimately find potential interventions and promote health in older adults (11). In this perspective paper, we will describe SARS-CoV-2 properties; then we will focus in the relationship between SARS-CoV-2 and aging, discussing the potential roles of comorbidities, inflammaging, immunosenescence, and immune escape. Finally, we will introduce Geroscience as a global approach to treat and prevent the onset and decrease the severity of diseases during aging, notably COVID-19. SARS-CoV-2 properties Coronaviruses are members of the Coronaviridae family. They are divided into Alphacoronavirus and Betacoronavirus that can only infect mammals, and Gammacoronavirus and Deltacoronavirus which mostly infect birds (1). SARS-CoV-2 is a Betacoronavirus (subgroup B Sarbecovirus), enveloped, with a positive single-stranded large RNA that can infect animals and humans. As MERS-CoV and SARS-CoV, it may cause severe diseases and high fatality rate....

Optimality in COVID-19 vaccination strategies determined by heterogeneity in human-human interaction networks

“…A general limiting factor in disease modelling, which also holds true for this work, is that the transition probabilities for the propagation of e.g. COVID-19 are intrinsically incomplete and evolving (Supplementary Table 24, [25][26][27][28][29]. A caveat in our study is the setting of relatively small European communities with a limited number of schools, work-and public places.…”

Immunesenescence: A Predisposing Risk Factor for the Development of COVID-19?

“…Thus, an increased presence of senescent cells may predispose to the development of severe COVID-19 via two mechanisms: ( 1 ) reduced immune cell clearance by contributing to the aforementioned inflammation-induced suppression of innate and adaptive immunity ( 204 , 205 , 225 ) and ( 3 ) increasing viral load by acting as a site of enhanced SARS-CoV-2 replication. Interestingly, a number of clinical trials assessing the therapeutic benefit of drugs that directly eliminate senescent cells or suppress their SASP are already underway in patients with COVID-19 ( 223 , 226 ). Results of such studies will help researchers address whether a high senescent cell burden is indeed a risk factor for the development of severe COVID-19.…”

Alterung von Lunge und Immunsystem als Meilensteine in der Pathogenese von idiopathischer Lungenfibrose und COVID-19

“…Ältere Menschen weisen eine höhere Viruslast und schwerere Verläufe auf [ 23 ] auf. Die oben beschriebenen Veränderungen im Rahmen der Lungenalterung haben einen wichtigen Anteil an der hohen Morbidität und Mortalität von COVID-19 im Alter.…”