**3. Pulmonary Fibrosis in Lung Transplant Recipients after COVID-19**

Follow-up data on the outcomes among lung transplant recipients who survived COVID-19 are scarce. Persistent post-COVID-19 parenchymal opacities (*n* = 29, 65.9%) could be demonstrated in chest CT in a majority of the lung transplant recipients who survived COVID-19 [7]. Significant loss of lung function was also observed in this population (*n* = 18, 40.9%), in which three patients (5.6%) developed chronic lung allograft dysfunction (CLAD), all three with the restrictive allograft syndrome (RAS) phenotype [7]. These patients typically had low absolute lymphocyte counts (<0.6 × 103/dl) and elevated ferritin levels (>150 ng/mL) [7]. Generally, the association between respiratory viral infections and the development of CLAD is suggested to be stronger in the case of symptomatic viral infections [8–11]. In one study asymptomatic respiratory viral infections were not associated with a significant decline in lung function [11,12]. If this also holds true for SARS-CoV-2 infections currently is unknown. In immunocompetent patients, pulmonary fibrosis four months after COVID-19 has been shown to be associated with the severity of illness [13]. In lung transplant recipients, however, these data are still lacking.
