Age is one of the principal risk factors in the majority of chronic illnesses such as cancer, diabetes, and heart disease. The COVID-19 pandemic has demonstrated the particular vulnerabilities of elderly people. Reducing the impact of age may, therefore, allow more effective treatment of SARS-CoV-2.
Cellular senescence is the biological process of cell aging, which causes modifications in their morphology, their gene expression, and their metabolism, and confers a certain resistance to programmed cell death (apoptosis). The senescent cells accumulate with age and secrete pro-inflammatory factors leading to chronic inflammation in elderly people. American researchers (at the University of Minnesota, Robert and Arlene Kogod Center on Aging, Rochester) have shown that these cells may be a cause of numerous harmful consequences of COVID-19 in elderly patients, and that new medicines that allow senescent cells to be eliminated may reduce serious cases.
The researchers firstly analysed the in vitro response of senescent cells when infection by a pathogen was simulated. They thus showed that senescent cells have much greater expression of inflammatory factors in response to infection than healthy cells. They then simulated infection with the spike protein of SARS-CoV-2, also in vitro, and came to the same conclusions.
In order to determine if results would be identical in vivo, the scientists simulated infection in young and old mice. The preceding results were confirmed: the senescent cells have a hyper-inflammatory response to infection. In addition, there was much greater mortality in the older mice than the younger ones when infection took place.