SARS-CoV-2, immunosenescence and inflammaging: partners in the COVID-19 crime

Abstract

Pneumonia outbreak in the city of Wuhan, China, prompted the finding of a novel strain of severe acute respiratory syndrome virus (SARS-CoV-2). Here, we discuss potential long-term consequences of SARS-CoV-2 infection, and its possibility to cause permanent damage to the immune system and the central nervous system. Advanced chronological age is one of the main risk factors for the adverse outcomes of COVID-19, presumably due to immunosenescence and chronic low-grade inflammation, both characteristic of the elderly. The combination of viral infection and chronic inflammation in advanced chronological age might cause multiple detrimental unforeseen consequences for the predisposition and severity of neurodegenerative diseases and needs to be considered so that we can be prepared to deal with future outcomes of the ongoing pandemic.

Keywords: COVID-19; SARS-CoV-2; aging; immunosenescence; inflammaging; neuroinflammation.

Figure 1

SARS-CoV-2 spike protein binds to the ACE2 receptor to enter the cells. Viral spike protein binds to the ACE2 receptor in the human cell membrane, followed by the internalization of the virus. SARS-CoV-2 consists also of the ribonucleoprotein, envelope protein and a membrane protein. The image was generated using CellPAINT Software [100].

Figure 2

Immunosencescence and inflammaging create a vicious cycle creating an environment favorable for the development of neurodegenerative diseases. Such a relationship between these processes is mainly characteristic of the elderly and is the most likely reason for the increased incidence and adversity of COVID-19 among the elderly.