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Abstract
Human cytomegalovirus (CMV) devotes substantial genomic capacity to evasion and modulation of host immunity, enabling lifelong persistence with minimal pathology in healthy hosts. Because CMV infects antigen‑presenting cells such as dendritic cells and macrophages, it can directly manipulate key immune signaling networks. This work establishes a rat CMV bone marrow–derived dendritic cell (BMDC) infection model and identifies a novel mechanism by which rat CMV downregulates MHC class II expression in these cells. In addition, two complementary model systems are developed to investigate cell‑type–specific viral tropism, elucidating its role in the CMV life cycle and the establishment of viral persistence.