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Background: Lymphopenia, particularly when restricted to the T-cell compartment, has been described as one of the major clinical hallmarks in patients with coronavirus disease 2019 (COVID-19) and proposed as an indicator of disease severity. Although several mechanisms fostering COVID-19-related lymphopenia have been described, including cell apoptosis and tissue homing, the underlying causes of the decline in T-cell count and function are still not completely understood., Objective: Given that viral infections can directly target thymic microenvironment and impair the process of T-cell generation, we sought to investigate the impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on thymic function., Methods: We performed molecular quantification of T-cell receptor excision circles and κ-deleting recombination excision circles to assess, respectively, T- and B-cell neogenesis in SARS-CoV-2-infected patients. We developed a system for in vitro culture of primary human thymic epithelial cells (TECs) to mechanistically investigate the impact of SARS-CoV-2 on TEC function., Results: We showed that patients with COVID-19 had reduced thymic function that was inversely associated with the severity of the disease. We found that angiotensin-converting enzyme 2, through which SARS-CoV-2 enters the host cells, was expressed by thymic epithelium, and in particular by medullary TECs. We also demonstrated that SARS-CoV-2 can target TECs and downregulate critical genes and pathways associated with epithelial cell adhesion and survival., Conclusions: Our data demonstrate that the human thymus is a target of SARS-CoV-2 and thymic function is altered following infection. These findings expand our current knowledge of the effects of SARS-CoV-2 infection on T-cell homeostasis and suggest that monitoring thymic activity may be a useful marker to predict disease severity and progression., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Objectives: To determine the value of surgery for infective endocarditis (IE) in patients on hemodialysis by comparing the nature and invasiveness of endocarditis in hemodialysis and nonhemodialysis patients and their hospital and long-term outcomes, and identifying risk factors for time-related mortality after surgery., Methods: From January 1997 to January 2013, 144 patients on chronic hemodialysis and 1233 nonhemodialysis patients underwent valve surgery for IE at our institution. Propensity matching identified 99 well-matched hemodialysis and nonhemodialysis patient pairs for comparison of outcomes., Results: Staphylococcus aureus infection was more common in hemodialysis patients than in nonhemodialysis patients (42% vs 21%; P < .0001), but invasive disease was similar in the 2 groups (47%; P = .3). Hospital mortality was 13% and 5-year survival was 20% for hemodialysis patients, 20% below that expected in a general hemodialysis population but 15% above that of hemodialysis patients treated nonsurgically for IE. For matched patients, hospital mortality was 13% for hemodialysis patients versus 5.1% for nonhemodialysis patients (P = .05), and survival at 1 and 5 years was 56% versus 83% and 24% versus 59%, respectively (P < .004). Use of an arteriovenous graft for dialysis access (P = .01) and preoperative placement of a pacemaker (P < .0001) were risk factors for late mortality in hemodialysis patients. For matched patients, freedom from reoperation was similar in the hemodialysis and nonhemodialysis groups (P > .9)., Conclusions: Intermediate-term survival after surgery for IE in hemodialysis patients is substantially worse than that in nonhemodialysis patients, but only slightly worse than that in the general hemodialysis population and substantially better than that in hemodialysis patients with IE treated nonsurgically, supporting continued surgical intervention for IE., (Copyright © 2017. Published by Elsevier Inc.)