Immune evasion proteins enhance cytomegalovirus latency in the lungs.
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.
Böhm
Verena
V
Institute for Virology, University Medical Center of Johannes Gutenberg University, 55131 Mainz, Germany.
Seckert
Christof K
CK
Simon
Christian O
CO
Thomas
Doris
D
Renzaho
Angélique
A
Gendig
Dorothea
D
Holtappels
Rafaela
R
Reddehase
Matthias J
MJ
D000818:Animals; D000938:Antigen-Presenting Cells / Q000821:virology; D001854:Bone Marrow Cells / Q000166:cytology; D018414:CD8-Positive T-Lymphocytes / Q000821:virology*; D003587:Cytomegalovirus / Q000378:metabolism*; D003586:Cytomegalovirus Infections / Q000821:virology; D005260:Female; D016679:Genome, Viral; D006023:Glycoproteins / Q000378:metabolism; D008168:Lung / Q000821:virology; D051379:Mice; D008807:Mice, Inbred BALB C; D012008:Recurrence; D014158:Transcription, Genetic; D017735:Virus Latency
D006023:Glycoproteins