Immunotherapy of cytomegalovirus infection by low-dose adoptive transfer of antiviral CD8 T cells relies on substantial post-transfer expansion of central memory cells but not effector-memory cells.
PLoS pathogens
View this publicationInstitute for Virology
University Hospital Bonn Venusberg-Campus 1, 53127 Bonn
The host-specific cytomegaloviruses (CMV) are large DNA viruses of the beta herpesvirus family. After acute infection, CMV genomes remain in a state of replicative latency in host tissues for life, interrupted by episodes of transcriptional reactivation. The establishment of latency is the result of a long period of co-evolution between CMV and its host. During this time, the virus and host have developed a fine balance of immune evasion and immune control to maintain latency. Under conditions of immunosuppression, productive infection can occur by reactivation of the productive cycle of latent genomes. Primary infection or reactivation can lead to life-threatening diseases, e.g. interstitial pneumonia in immunocompromised patients after haematopoietic (stem) cell transplantation (HCT).
The main research topic of our group is to study the establishment of acute and latent CMV infection in a mouse model. We aim to understand the molecular and immunological basis of CMV control by the immune system and the viral countermeasures that lead to the establishment of latency.