Publication date: Dec 05, 2024

The COVID-19 pandemic has led to significant morbidity and mortality in lung transplant recipients (LTR). Respiratory viral infections may be associated with de-novo HLA donor-specific antibody (DSA) production and impact lung transplant outcomes. Since one of the immunomodulation strategies post-SARS-CoV-2 infection in LTR include decreasing or holding anti-metabolites, concerns have been raised for higher incidence of de-novo DSA production in LTR. We performed a retrospective chart review of 63 consecutive LTR diagnosed with COVID-19 to investigate this concern. COVID-19 disease severity was divided into 3 groups: mild, moderate, and severe. Mild disease was defined as patients with COVID-19 diagnosis who were stable enough to be treated as out-patients. Moderate disease was defined as patients who required admission to the hospital and were on less than 10 l of oxygen at rest. Severe disease was identified as patients who required hospitalization and were on more than 10 l of oxygen with or without mechanical ventilation or extra corporal membrane oxygenation (ECMO). Groups were compared using the Kruskal-Wallis test. A total of 11, 43, and 9 LTR were diagnosed with mild, moderate, and severe COVID-19 respectively. We observed no significant differences in the CPRA pre-COVID-19 compared to 1 and 6 months post-COVID-19 diagnosis in 6/11 (54. 5 %), 18/43 (41. 8 %), and 6/9 (66. 9 %) LTR with mild (p = 0. 66), moderate (p = 0. 74), and severe (p = 0. 22) COVID-19 respectively. HLA class I and II DSA were detected pre-COVID-19 diagnosis and persisted with no significant differences in the median MFI levels at 1 and 6 months post-COVID-19 diagnosis in 2/11 (p = 0. 93), 7/43 (p = 0. 71), and 0/9 LTR with mild, moderate, and severe COVID-19 respectively. De-novo HLA DSA were detected within 6 months post-COVID-19 diagnosis in 0/11 (0 %), 1/43 (2. 3 %), and 3/9 (33. 3 %%) LTR with mild, moderate, and severe COVID-19 respectively (p = 0. 001). Severe COVID-19 may be associated with increased risk of de novo HLA DSA production resulting in allograft dysfunction.

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