scholarly journals COVID-19 and Crosstalk between the Hallmarks of Aging

Author(s):  
Shabnam Salimi ◽  
John M. Hamlyn

Within the past several decades, the emergence of new viral diseases with more severe health complications and mortality, primarily in older adults with comorbidities, is evidence of an age-dependent, compromised bodily response to abrupt stress with concomitant reduced immunity. The emergence of new infectious coronaviruses such as SARS-CoV-2 has resulted in the coronavirus disease 2019 (COVID-19). The result is increased morbidity and mortality in persons with underlying chronic diseases and among those with compromised defense mechanisms, regardless of age and among older adults who are more likely to fit these categories. COVID-19 appears to be primarily an upper respiratory disease. 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 (ARDS), lung fibrosis, cardiac t complication, acute kidney injury, hospitalization, and high mortality have been reported in older adults with COVID-19, that result from pathogen-host interactions. Here, we review potential interactions of the coronavirus and host cellular responses in relation to hallmarks of aging including genomic instability, telomere attrition, impaired autophagy, mitochondrial dysfunction, innate immunosenescence, inflammation and inflammasomes, adaptive immunosenescence, and epigenetic alterations, that likely contribute to the increased pathophysiological responses to SARS-CoV-2 among older adults.

2020 ◽  
Vol 75 (9) ◽  
pp. e34-e41 ◽  
Author(s):  
Shabnam Salimi ◽  
John M Hamlyn

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.


Author(s):  
Shabnam Salimi ◽  
John M. Hamlyn

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, telomere attrition, epigenetic alterations, 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 anti-aging drug candidates that require paramount attention in COVID-19 research.


Author(s):  
Ashley Lytle ◽  
MaryBeth Apriceno ◽  
Jamie Macdonald ◽  
Caitlin Monahan ◽  
Sheri R Levy

Abstract Objectives During the coronavirus disease 2019 (COVID-19) pandemic, older adults have been disproportionately affected by high rates of health complications and mortality. Reactions toward older adults included a mix of prosocial behaviors and ageist responses, consistent with the history of positive and negative views and treatment of older adults in the United States. Methods In a two-part study (n = 113, Mage = 18.49, SD = 0.50; range 18–19), we examined whether pre-pandemic ageism among undergraduates predicts prosocial behavioral intentions toward older adults both specific to COVID-19 and in general. Results Pre-pandemic ageism toward older adults predicted less intentions to help older adults generally and specific to COVID-19. Whereas viewing older adults as incompetent predicted greater intentions to help specific to COVID-19. Discussion These results reflect the complexity of predicting helping behaviors and suggest that even supportive behaviors toward older adults during the COVID-19 pandemic may be rooted in negative ageist stereotypes. Implications and directions for future research are discussed.


2020 ◽  
Author(s):  
Angélica Arcanjo ◽  
Jorgete Logullo ◽  
Paulo Emílio Corrêa Leite ◽  
Camilla Cristie Barreto Menezes ◽  
Celio Geraldo Freire-de-Lima ◽  
...  

Abstract COVID-19 is a disease caused by the novel SARS-CoV-2 coronavirus, originally classified as a severe acute respiratory syndrome coronavirus (SARS-CoV). The most severe cases of COVID-19 can progress to severe pneumonia with respiratory failure, septicemia, multiple organ failure and death. The severity of the disease is aggravated by the deregulation of the immune system causing an excessive initial inflammation including the cytokine storm, compring interleukins characteristic of the T-dependent adaptive response. In the present study we show that severe patients have high levels of T helper type-1 and type-2 cytokines, as well as VGEF. Furthermore, our show abnormal cytokine levels upon T-cell mitogen stimulation, in a non-polarized response profile. This response is not specific, given that the stimulus with the heterologous tuberculin antigen was able to induce high levels of cytokines compared to healthy controls, including the vascular endothelial growth factor VEGF, which promotes neoangiogenesis in physiological and pathophysiological conditions, caused by tissue hypoxia, and involved in a clonal exhaustion program in T cells. This can be decisive given our findings demonstrating for the first time a significantly increased frequency of late-differentiated CD8+ T cells characterized by critically shortened telomeres with particular phenotype (CD57+CD28-) in severe acute COVID-19 infection. These findings reveal that severe COVID-19 is associated with senescence of T cells, especially within the CD8+ T cell compartment and points to possible mechanisms of loss of clonal repertoire and susceptibility to recurrences of COVID-19 symptoms, due to viral relapse and reinfection events.


2018 ◽  
Vol 5 (9) ◽  
Author(s):  
Catharine Chambers ◽  
Danuta M Skowronski ◽  
Caren Rose ◽  
Gaston De Serres ◽  
Anne-Luise Winter ◽  
...  

Abstract We investigated sex as a potential modifier of influenza vaccine effectiveness (VE) between 2010–2011 and 2016–2017 in Canada. Overall VE was 49% (95% confidence interval [CI], 43% to 55%) for females and 38% (95% CI, 28% to 46%) for males (absolute difference [AD], 11%; P = .03). Sex differences were greatest for influenza A(H3N2) (AD, 17%; P = .07) and B(Victoria) (AD, 20%; P = .08) compared with A(H1N1)pdm09 (AD, 10%; P = .19) or B(Yamagata) (AD, –3%; P = .68). They were also more pronounced in older adults ≥50 years (AD, 19%; P = .03) compared with those <20 years (AD, 4%; P = .74) or 20–49 years (AD, –1%; P = .90) but with variation by subtype/lineage. More definitive investigations of VE by sex and age are warranted to elucidate these potential interactions.


2012 ◽  
Author(s):  
Ali J. Olyaei ◽  
William M. Bennett

Prescribing drugs in patients with kidney disease is complex: drug dosing needs to be adjusted by the stage of kidney disease (whether chronic kidney disease [CKD] stages 1 through 5 or acute kidney injury [AKI] stages 1 through 3); because potential interactions with other agents that are being used need to be considered; and because of the possibility of extracorporeal treatment that might need to be used (e.g., continuous renal replacement therapy [CRRT], peritoneal dialysis [PD], or hemodialysis [HD]). Besides this complexity, there has been an explosion in the classes of new agents and the routes of delivery of these agents. The purpose of this chapter is to review the basic pharmacokinetic and pharmacologic principles that should guide therapy and to summarize basic recommendations for patients with CKD and AKI. The general principles for drug dosing in CKD and AKI include pharmacokinetics in renal failure; bioavailability; volume of distribution; protein binding; and biotransformation. A stepwise approach to dosage adjustment is described and created as an algorithmic approach. Drug dosing considerations in dialysis patients and in AKI patients are covered as well. This chapter contains 2 algorithms, 7 tables, 25 references, 5 Board-styled MCQs, and 1 Teaching Slide Set.


Author(s):  
Natalie Ebert ◽  
Elke Schaeffner

Both acute and chronic states of kidney disease have considerable healthcare impact as they can produce enormous disease burden and costs. To classify chronic kidney disease into the CKD staging system, glomerular filtration rate as an index of kidney function, as well as albuminuria as a marker of kidney damage have to be assessed as correctly as possible. Misclassification is a serious concern due to the difficulties in precise GFR assessment and correct interpretation of results. Differentiating between pure senescence and true disease among older adults can be a delicate issue. To find the right renal replacement option for individuals that progress to end-stage renal disease can be challenging, and some older patients may even benefit from conservative care without dialysis. To prevent acute kidney injury as a frequent and potentially life-threatening complication, clinicians need to develop an understanding of the common vulnerability to kidney damage among older adults.


Sign in / Sign up

Export Citation Format

Share Document