Human herpesvirus 6B induces cell cycle arrest concomitant with p53 phosphorylation and accumulation in T cells.
We studied the interactions between human herpesvirus 6B (HHV-6B) and its host cell. Productive infections of T-cell lines led to G1/S- and G2/M-phase arrest in the cell cycle concomitant with an increased level and enhanced DNA-binding activity of p53. More than 70% of HHV-6B-infected cells did not bind annexin V, indicating that the majority of cells were not undergoing apoptosis. HHV-6B infection induced Ser20 and Ser15 phosphorylation on p53, and the latter was inhibited by caffeine, an ataxia telangiectasia mutated kinase inhibitor. Thus, a productive HHV-6B infection suppresses T-cell proliferation concomitant with the phosphorylation and accumulation of p53.
Øster
Bodil
B
Department of Medical Microbiology and Immunology, Bartholin Building, University of Aarhus, DK-8000 Aarhus C, Denmark.
Bundgaard
Bettina
B
Höllsberg
Per
P
D002453:Cell Cycle / Q000502:physiology*; D002460:Cell Line; D004268:DNA-Binding Proteins / Q000378:metabolism; D015654:Herpesvirus 6, Human / Q000472:pathogenicity*; D006801:Humans; D010766:Phosphorylation; D019349:Roseolovirus Infections / Q000821:virology; D013601:T-Lymphocytes / Q000166:cytology / Q000378:metabolism / Q000821:virology*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
D004268:DNA-Binding Proteins; D016159:Tumor Suppressor Protein p53