Cell Cycle Arrest during Measles Virus Infection: a G0-Like Block Leads to Suppression of Retinoblastoma Protein Expression

摘要: One of the major mechanisms by which measles virus (MV) infection causes disease and death is suppression immune response. The nonresponsiveness MV-infected human lymphocytes to mitogens a partial block in G0/G1 phase cell cycle observed vitro thought reflect vivo immunosuppression. In order molecularly dissect MV-induced immunosuppression, we analyzed expression surface activation markers cycle-regulatory proteins T lymphocytes. MV Edmonston (MV-Ed) could induce maintain high level early marker CD69 absence proliferation. Expression cyclins D3 E, positively control entry into S phase, was also significantly decreased. Analysis inhibitors progression showed that p27 maintained G0/G1-blocked subpopulation MV-Ed-infected cells compared proliferating cells. Furthermore, cycle-related upregulation retinoblastoma (Rb) protein synthesis did not occur Acridine orange staining, distinguishes G0 from G1, RNA levels were upregulated following activation, consistent with remaining state. Although indicated cycle, intracellular Rb suggested quiescent These results indicate can uncouple transition G1.