ABSTRACT
BACKGROUND: Serological responses to COVID-19 vaccination are diminished in recipients of solid organ transplants, especially in lung transplant recipients (LTR), probably as result of immunosuppressive treatment. There is currently no marker of immunosuppression that can be used to predict the COVID-19 vaccination response. Here, we study whether torque tenovirus (TTV), a highly prevalent virus can be used as an indicator of immunosuppression. METHODS: The humoral response to the mRNA 1273 vaccine was assessed in 103 LTR, who received a transplant between 4 and 237 months prior to vaccination, by measuring Spike (S)-specific IgG levels at baseline, 28 days after first, and 28 days after the second vaccination. TTV loads were determined by RT-PCR and Pearson's correlation coefficient was calculated to correlate serological responses to TTV load. RESULTS: Humoral responses to COVID-19 vaccination were observed in 41 of 103 (40%) LTR at 28 days after the second vaccination. Sixty-two of 103 (60%) were non-responders. Lower TTV loads at baseline (significantly) correlated with higher S-specific antibodies and a higher percentage of responders. Lower TTV loads also strongly correlated with longer time since transplantation, indicating that participants with lower TTV loads were longer after transplantation. CONCLUSIONS: This study shows a better humoral response to the SARS-CoV-2 vaccine in subjects with a lower TTV load pre-vaccination. In addition, TTV load correlates with the time after transplantation. Further studies on the use of TTV load in vaccination efficacy studies in immunocompromised cohorts should provide leads for the potential use of this marker for optimizing vaccination response.
Subject(s)
COVID-19 , Torque teno virus , 2019-nCoV Vaccine mRNA-1273 , COVID-19/prevention & control , COVID-19 Vaccines , Humans , Lung , SARS-CoV-2 , Torque , Torque teno virus/genetics , Transplant Recipients , VaccinationABSTRACT
We report a patient with COVID-19 requiring hospitalization for two weeks, complicated by multiple segmental pulmonary embolisms for which dabigatran was initiated. After clearing the infection, the patient remained asymptomatic for 5 months. He was then readmitted with a spontaneous haemothorax, most likely related to the use of dabigatran, which progressed to a pleural empyema with a trapped lung. The patient underwent a video assisted thoracoscopy (VATS) with decortication. Because of focal abnormalities, biopsies for histopathology were taken from the lung parenchyma. These showed an organizing pneumonia with progression towards fibrosis and arteries with intimal fibrosis. So far, no histopathological reports exist on late pulmonary changes after a COVID-19 infection. The unusual combined presence of microvascular damage and interstitial fibrosis may reflect a pathophysiological concept in which early endothelial damage by SARS-CoV-2 can lead to a chronic state of microvascular damage, low grade inflammation, and early progression towards pulmonary fibrosis.