COVID-19 and Crosstalk With the Hallmarks of Aging

Abstract

Within the past several decades, the emergence of new viral diseases with severe health complications and mortality is evidence of an age-dependent, compromised bodily response to abrupt stress with concomitantly reduced immunity. The new severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, causes coronavirus disease 2019 (COVID-19). It has increased morbidity and mortality in persons with underlying chronic diseases and those with a compromised immune system regardless of age and in older adults who are more likely to have these conditions. While SARS-CoV-2 is highly virulent, there is variability in the severity of the disease and its complications in humans. Severe pneumonia, acute respiratory distress syndrome, lung fibrosis, cardiovascular events, acute kidney injury, stroke, hospitalization, and mortality have been reported that result from pathogen–host interactions. Hallmarks of aging, interacting with one another, have been proposed to influence health span in older adults, possibly via mechanisms regulating the immune system. Here, we review the potential roles of the hallmarks of aging, coupled with host–coronavirus interactions. Of these hallmarks, we focused on those that directly or indirectly interact with viral infections, including immunosenescence, inflammation and inflammasomes, adaptive immunosenescence, genomic instability, mitochondrial dysfunction, epigenetic alterations, telomere attrition, and impaired autophagy. These hallmarks likely contribute to the increased pathophysiological responses to SARS-CoV-2 among older adults and may play roles as an additive risk of accelerated biological aging even after recovery. We also briefly discuss the role of antiaging drug candidates that require paramount attention in COVID-19 research.

Association of Herpesvirus Response Burden with Long-Term Mortality Differs Between Older Males and Females

“…Typical common intracellular microbes with readily available serologic testing and Since long-term mortality data of Covid- 19 are not yet available, this prompted us to investigate whether sex differences in mortality would apply to other common infections. We tested associations between immunoglobulin G (IgG) antibody titers for HSV-1, HSV-2, CMV, C. pneumoniae, M. pneumonia and H. pylori and long-term mortality among persons aged ≥75 years, a group of people who are especially vulnerable to Covid-19 through numerous pathophysiological mechanisms related to ageing [11]. Besides being old and past reproductive age, our study subjects were community-dwelling and had a history of cardiovascular disease (CVD), which reduces the possibility that gender-patterned factors related to environment, lifestyle, current hormonal, and cardiovascular status would explain the findings.…”

Epidemiological profile of COVID-19 deaths in the public hospital in Rio de Janeiro, Brazil

“…COVID-19 show significant host factors for replication which are impacted by age coupled with comorbidities and immune system responses that enhance the severity of the viral infection. 16 Hence, it has been observed that the alveolar lesions occur in a variety of forms such as exudative inflammation, carnification, interstitial inflammation, fibrosis as well as focal hemorrhage. 17 Our study showed that deaths due to COVID-19 occurred in patients aged ≥60years.…”

COVID-19 Disease Map, a computational knowledge repository of SARS-CoV-2 virus-host interaction mechanisms

“…SARS-CoV-2 infection is associated with increased morbidity and mortality in individuals with underlying chronic diseases or a compromised immune system [225][226][227][228]. Groups of increased risk are men, pregnant and postpartum women, and individuals with high occupational viral exposure [229][230][231].…”

“…Importantly, age is one of the key aspects contributing to the severity of the disease. The elderly are at high risk of developing severe or critical disease [227,247]. Age-related elevated levels of pro-inflammatory cytokines (inflammation) [247][248][249][250], immunosenescence and cellular stress of ageing cells [125,227,247,251,252] may contribute to the risk.…”

“…The elderly are at high risk of developing severe or critical disease [227,247]. Age-related elevated levels of pro-inflammatory cytokines (inflammation) [247][248][249][250], immunosenescence and cellular stress of ageing cells [125,227,247,251,252] may contribute to the risk. In contrast, children are generally less likely to develop severe disease [253,254], with the exception of infants [125,[255][256][257].…”