Immune Evasion Proteins Enhance Cytomegalovirus Latency in the Lungs

被引:16
作者
Boehm, Verena [1 ]
Seckert, Christof K. [1 ]
Simon, Christian O. [1 ]
Thomas, Doris [1 ]
Renzaho, Angelique [1 ]
Gendig, Dorothea [1 ]
Holtappels, Rafaela [1 ]
Reddehase, Matthias J. [1 ]
机构
[1] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Inst Virol, D-55131 Mainz, Germany
关键词
CD8; T-CELLS; BONE-MARROW-TRANSPLANTATION; CLASS-I COMPLEXES; MURINE CYTOMEGALOVIRUS; ANTIGEN PRESENTATION; LYMPHOCYTES-T; TRANSCRIPTIONAL REACTIVATION; IMMUNOCOMPROMISED HOST; ADOPTIVE TRANSFER; INFECTED DONORS;
D O I
10.1128/JVI.01143-09
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页码:10293 / 10298
页数:6
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