Simian virus 40 infection disrupts p130-E2F and p107-E2F complexes but does not perturb pRb-E2F complexes

Virology. 2004 Mar 15;320(2):218-28. doi: 10.1016/j.virol.2003.10.035.


In its native host species, the Rhesus Macaque, simian virus 40 (SV40) forms a persistent infection in the kidneys with no apparent harmful side effects. We show that SV40 infection of growth-arrested monkey kidney epithelial cells results in the specific disruption of certain Rb-E2F family complexes. Throughout the course of infection, p130-E2F and p107-E2F complexes are disrupted, but surprisingly pRb-E2F complexes remain intact. This suggests that the presence of some pRb-E2F complexes is not inhibitory to productive infection. Additionally, while a decrease of p130 steady state levels is observed during the later time points of infection, early during infection, p130 is readily detectable. This suggests SV40 infection overrides p130-mediated growth arrest through a mechanism(s) in addition to the well-documented T antigen-mediated degradation of p130. Finally, infection induces a dramatic relocalization of E2F4 from the nucleus to the cytoplasm. The implications of these observations to the life cycle of the virus are addressed.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adaptor Proteins, Vesicular Transport / metabolism*
  • Animals
  • Cell Cycle Proteins*
  • Cell Line
  • DNA-Binding Proteins*
  • E2F Transcription Factors
  • Kidney / cytology
  • Nuclear Proteins / metabolism
  • Phosphoproteins / metabolism*
  • Proteins*
  • Retinoblastoma Protein / metabolism*
  • Retinoblastoma-Like Protein p130
  • Simian virus 40 / metabolism
  • Simian virus 40 / pathogenicity*
  • Transcription Factors / metabolism*


  • Adaptor Proteins, Vesicular Transport
  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • E2F Transcription Factors
  • Nuclear Proteins
  • Phosphoproteins
  • Proteins
  • Retinoblastoma Protein
  • Retinoblastoma-Like Protein p130
  • Transcription Factors