Does infection with SARS-CoV-2 increase immune ageing?

Abstract

ABSTRACT Background: The coronavirus disease 2019 (2019) pandemic caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), a viral respiratory infection, causes several defects in the immune system that appear to be similar to those observed in the immune system of older people, especially during the acute stages of the COVID-19. Therefore, the hypothesis has been raised that SARS-CoV-2 causes accelerated ageing of the immune system. Methods: Markers of differentiation and senescence on T cells, B cells, NK cells, and monocytes were examined using flow cytometry from 15 patients with mild cases and 8 patients with severe cases of COVID-19 at three months post-infection compared with 15 age-matched healthy controls. The immune system age of COVID-19 patients and healthy controls was measured using the IMM-AGE scores approach. Findings: The results suggest that SARS-CoV-2 infection has a lasting influence on the immune system in terms of reducing the frequency of CD8+CD45RA+CCR7+ T cells, CD8+CCR7+CD45RA− T cells, CD19+ B cells, CD19+CD24+CD38+ B cells, and CD14−CD16+ monocytes, especially in patients recovering from severe cases of COVID-19. Moreover, an examination of senescence markers on lymphocytes revealed that patients with severe COVID-19 showed a reduction in the frequencies of NKG2D and KLRG1 positive CD4+ and CD8+ T cells compared with healthy controls. Furthermore, the expression of NKG2D+ NK cells was decreased in patients with both mild and severe cases who recovered from COVID-19 compared with healthy individuals. Additionally, measuring the age of the immune system revealed that patients recovering from COVID-19 had an immune age that was older than their chronological age, and a comparison between a cohort of patients recovering from mild COVID-19 with an age-matched healthy cohort revealed comparable results. Conclusion: Our observations suggest that apart from the persistence of lymphocyte subsets depletion in patients recovering from severe COVID-19, abnormal senescence phenotypes in lymphocytes could be temporary and restored in patients recovering from COVID-19. However, the verification of existing observations requires confirmation in a broader patient population.