Purpose of review: Lung transplantation is an established therapeutic option for patients with severe respiratory insufficiency. Graft dysfunction or rejection depends on the orchestrated prevention of infection(s) and the level of immune suppression. More recent reports underlined the role and pathogenicity of cytomegalovirus (CMV) infection in lung transplant recipients and the double-edged sword of maintaining antiviral immune responses versus guided immune suppression to avoid graft rejection. We present data concerning the nature of the cellular response to Epstein-Barr virus (EBV) and CMV, the subsequent use of cellular therapy in antiviral treatment modalities and discuss the role of H1N1 infection and other viral infections in lung transplantation recipients.
Recent findings: Patients after lung transplantation showed a similar susceptibility to H1N1 infections as compared to the local, healthy community. After initial recovery and oseltamivir treatment, lung transplantation patients developed bronchiolitis obliterans syndrome. The genetic background of lung transplant recipients, defined by polymorphism in immune molecules, contributes to increased risk of CMV disease; CMV induces local pro-inflammatory chemokines (CXCL10). Anti-CMV prophylaxis does not impact on anti-CMV-directed cellular immune responses, defined by IFNγ and TNFα production. Asymptomatic EBV carriers showed higher numbers of EBV-reactive T cells. High EBV load carriers showed T cells with immune-exhaustion markers and decreased IFNγ production. Anti-CMV-directed cellular therapy may aid to better manage CMV-associated complications after lung transplantation.
Summary: Pharmacological immune suppression, the genetic makeup of the patient as well as concurrent viral infections impact on the successful outcome of lung transplantation and call for more detailed immune-guided diagnostics and therapy.