Measles virus V protein inhibits p53 family member p73

Cristian D. Cruz, Heidi Palosaari, Jean Patrick Parisien, Patricia Devaux, Roberto Cattaneo, Toru Ouchi, Curt M. Horvath

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


Paramyxovirus V proteins function as host interference factors that inactivate antiviral responses, including interferon. Characterization of cellular proteins that copurify with ectopically expressed measles virus V protein has revealed interactions with DNA binding domains of p53 family proteins, p53 and p73. Specific transcriptional assays reveal that expression of measles virus V cDNA inhibits p73, but not p53. Expression of measles virus V cDNA can delay cell death induced by genotoxic stress and also can decrease the abundance of the proapoptotic factor PUMA, a p73 target. Recombinant measles virus with an engineered deficiency in V protein is capable of inducing more severe cytopathic effects than the wild type, implicating measles virus V protein as an inhibitor of cell death. These findings also suggest that p73-PUMA signaling may be a previously unrecognized arm of cellular innate antiviral immunity.

Original languageEnglish (US)
Pages (from-to)5644-5650
Number of pages7
JournalJournal of virology
Issue number11
StatePublished - Jun 2006

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology


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