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RESEARCH PRODUCT
Immune Evasion Proteins Enhance Cytomegalovirus Latency in the Lungs
Matthias J. ReddehaseRafaela HoltappelsChristian O. SimonDorothea GendigChristof K. SeckertAngélique RenzahoDoris ThomasVerena Böhmsubject
Transcription GeneticImmunologyAntigen presentationAntigen-Presenting CellsCytomegalovirusBone Marrow CellsGenome ViralCD8-Positive T-LymphocytesBiologymedicine.disease_causeMicrobiologyHerpesviridaeVirusMiceImmune systemRecurrenceVirologyVirus latencymedicineAnimalsCytotoxic T cellAntigen-presenting cellLungGlycoproteinsMice Inbred BALB Cmedicine.diseaseVirologyVirus LatencyInsect ScienceCytomegalovirus InfectionsImmunologyPathogenesis and ImmunityFemaleViral diseasedescription
ABSTRACT CD8 T cells control cytomegalovirus (CMV) infection in bone marrow transplantation recipients and persist in latently infected lungs as effector memory cells for continuous sensing of reactivated viral gene expression. Here we have addressed the question of whether viral immunoevasins, glycoproteins that specifically interfere with antigen presentation to CD8 T cells, have an impact on viral latency in the murine model. The data show that deletion of immunoevasin genes in murine CMV accelerates the clearance of productive infection during hematopoietic reconstitution and leads to a reduced latent viral genome load, reduced latency-associated viral transcription, and a lower incidence of recurrence in lung explants.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2009-10-01 | Journal of Virology |