Viruses as hijackers of PML nuclear bodies.
Promyelocytic leukemia nuclear bodies (PML-NBs) are discrete interchromosomal macromolecular structures. The integrity of this dynamic nuclear subcompartment critically depends on the presence of the name-giving PML protein. Among the permanent or transient residents of PML-NBs are various regulatory proteins, including Sp100, CBP, pRb, HIPK2, RAD51 and p53. PML-NBs are frequently targeted by viral infections, as a number of different RNA and DNA viruses, including herpesviruses, adenoviruses, papovaviruses, papillomaviruses and arenaviruses, cause changes in PML-NBs. Viruses interfere with PML-NB in two ways: 1) some viral proteins can associate with PML-NB proteins and/or lead to the destruction and lysis of this subnuclear compartment, thus aiding viral gene expression and disabling the host's innate immunity; 2) the parental genomes of some nuclear-replicating DNA viruses associate preferentially with PML-NBs, which presumably serves to assist in viral gene expression or replication. Here we feature the different viral strategies leading to the hijacking of PML-NBs and discuss the consequences for the immune response.
Möller
Andreas
A
Department of Chemistry and Biochemistry, University of Bern, CH-3012 Bern, Switzerland.
Schmitz
M Lienhard
ML
D000818:Animals; D022003:Cell Nucleus Structures / Q000737:chemistry*; D006801:Humans; D007113:Immunity, Innate; D007372:Interferons / Q000494:pharmacology; D009363:Neoplasm Proteins / Q000737:chemistry / Q000502:physiology*; D009687:Nuclear Proteins; D015388:Organelles / Q000737:chemistry*; D000071156:Promyelocytic Leukemia Protein; D014157:Transcription Factors / Q000737:chemistry / Q000502:physiology*; D025521:Tumor Suppressor Proteins; D016662:Virus Integration; D014779:Virus Replication; D014780:Viruses / Q000472:pathogenicity*
D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D000071156:Promyelocytic Leukemia Protein; D014157:Transcription Factors; D025521:Tumor Suppressor Proteins; C070576:PML protein, human; D007372:Interferons