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.

严重急性呼吸系统综合症冠状病毒2（SARS-CoV-2）感染的特征是老年男性与年龄相关的合并症的高死亡率。在大多数这些患者中，不受控制的局部和全身性过度炎症会导致严重的甚至致命的后果。衰老过程的特征是慢性亚临床全身性炎症的逐渐发展（炎症衰老）和获得性免疫系统的损害（免疫衰老）。在这里，我们提出以下假设：衰老有四个公认的特征导致老年男性SARS-CoV-2死亡率过高。没有明显疾病的亚临床全身炎症的存在； ii。由于慢性发炎，后天免疫力下降和I型干扰素反应；iii。ACE2的下调（即SARS-CoV-2受体）；iv。加速生物衰老。SARS-CoV-2感染的高死亡率表明，阐明炎症衰老和免疫衰老的机制不仅可以帮助对抗与年龄有关的疾病，还可以帮助对抗SARS-CoV-2感染。