tetano
Editor, Senior Moderator
Cytokine Growth Factor Rev. 2020 May 3. pii: S1359-6101(20)30084-8. doi: 10.1016/j.cytogfr.2020.04.005. [Epub ahead of print]
Inflamm-aging: Why older men are the most susceptible to SARS-CoV-2 complicated outcomes.
Bonaf? M[SUP]1[/SUP], Prattichizzo F[SUP]2[/SUP], Giuliani A[SUP]3[/SUP], Storci G[SUP]1[/SUP], Sabbatinelli J[SUP]4[/SUP], Olivieri F[SUP]5[/SUP].
Author information
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is characterized by a high mortality of elderly men with age-related comorbidities. In most of these patients, uncontrolled local and systemic hyperinflammation induces severe and often lethal outcomes. The aging process is characterized by the gradual development of a chronic subclinical systemic inflammation (inflamm-aging) and by acquired immune system impairment (immune senescence). Here, we advance the hypothesis that four well-recognized features of aging contribute to the disproportionate SARS-CoV-2 mortality suffered by elderly men: i. the presence of subclinical systemic inflammation without overt disease, ii. a blunted acquired immune system and type I interferon response due to the chronic inflammation; iii. the downregulation of ACE2 (i.e. the SARS-CoV-2 receptor); and iv. accelerated biological aging. The high mortality rate of SARS-CoV-2 infection suggests that clarification of the mechanisms of inflamm-aging and immune senescence can help combat not only age-related disorders but also SARS-CoV-2 infection.
Copyright ? 2020 Elsevier Ltd. All rights reserved.
KEYWORDS:
COVID-19; Cardiovascular diseases; Host-directed therapies; Inflamm-aging; SARS-CoV-2; interleukin-6
PMID:32389499DOI:10.1016/j.cytogfr.2020.04.005
Inflamm-aging: Why older men are the most susceptible to SARS-CoV-2 complicated outcomes.
Bonaf? M[SUP]1[/SUP], Prattichizzo F[SUP]2[/SUP], Giuliani A[SUP]3[/SUP], Storci G[SUP]1[/SUP], Sabbatinelli J[SUP]4[/SUP], Olivieri F[SUP]5[/SUP].
Author information
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is characterized by a high mortality of elderly men with age-related comorbidities. In most of these patients, uncontrolled local and systemic hyperinflammation induces severe and often lethal outcomes. The aging process is characterized by the gradual development of a chronic subclinical systemic inflammation (inflamm-aging) and by acquired immune system impairment (immune senescence). Here, we advance the hypothesis that four well-recognized features of aging contribute to the disproportionate SARS-CoV-2 mortality suffered by elderly men: i. the presence of subclinical systemic inflammation without overt disease, ii. a blunted acquired immune system and type I interferon response due to the chronic inflammation; iii. the downregulation of ACE2 (i.e. the SARS-CoV-2 receptor); and iv. accelerated biological aging. The high mortality rate of SARS-CoV-2 infection suggests that clarification of the mechanisms of inflamm-aging and immune senescence can help combat not only age-related disorders but also SARS-CoV-2 infection.
Copyright ? 2020 Elsevier Ltd. All rights reserved.
KEYWORDS:
COVID-19; Cardiovascular diseases; Host-directed therapies; Inflamm-aging; SARS-CoV-2; interleukin-6
PMID:32389499DOI:10.1016/j.cytogfr.2020.04.005