Bordoni V, Tartaglia E, Sacchi A, et al. - Given that COVID-19 patients show significant suppression of Deacetylase Sirtuin 1 (SIRT1) which targets a variety of transcription factors, including p53, and SIRT1 was noted to negatively correlated with p53, researchers sought to determine the role and influence of p53 and deacetylase Sirtuin 1 (SIRT1) on lymph-monocyte homeostasis and their possible effect on T and B cell signalling. They performed gene expression analysis and flow cytometry on peripheral blood mononuclear cells of 35 COVID-19 patients and 10 healthy donors (HD). Relative to Healthy donors, COVID-19 patients had a significantly higher level of p21, an essential mediator of p53-dependent cell-cycle arrest. The loss of lymphocytes by apoptotic processes seems similar to that reported in patients with SARS-COV-1 infection during the 2003 SARS outbreak. Indirect mechanisms rather than direct viral infection/replication pathways may be mediating this. Levels of IL1 β, IL-6, IL-8 and TNF-α were higher in COVID-19 and there was positive correlation of inflammatory cytokines with p53 and negative correlation with SIRT-1. COVID-19 patients exhibited a significant lower BLNK expression, which was negatively linked with inflammatory cytokines and positively with SIRT-1. Findings overall suggest that in COVID-19 patients, cell survival, B cell signalling and antibody production are possibly affected by the inflammatory environment, the dysregulated p53/SIRT-1 axis and the low expression of key genes of lymphocytes homeostasis (IL7R and BLNK).