Chapter

NF-kB in Health and Disease

Volume 349 of the series Current Topics in Microbiology and Immunology pp 197-244

Date:

NF-κB as a Target for Oncogenic Viruses

  • Shao-Cong SunAffiliated withDepartment of Immunology, The University of Texas MD Anderson Cancer Center and The University of Texas Graduate School of Biomedical Sciences at Houston Email author 
  • , Ethel CesarmanAffiliated withDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College Email author 

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Abstract

NF-κB is a pivotal transcription factor that controls cell survival and proliferation in diverse physiological processes. The activity of NF-κB is tightly controlled through its cytoplasmic sequestration by specific inhibitors, IκBs. Various cellular stimuli induce the activation of an IκB kinase, which phosphorylates IκBs and triggers their proteasomal degradation, causing nuclear translocation of activated NF-κB. Under normal conditions, the activation of NF-κB occurs transiently, thus ensuring rapid but temporary induction of target genes. Deregulated NF-κB activation contributes to the development of various diseases, including cancers and immunological disorders. Accumulated studies demonstrate that the NF-κB signaling pathway is a target of several human oncogenic viruses, including the human T cell leukemia virus type 1, the Kaposi sarcoma-associated herpesvirus, and the Epstein–Bar virus. These viruses encode specific oncoproteins that target different signaling components of the NF-κB pathway, leading to persistent activation of NF-κB. This chapter will discuss the molecular mechanisms by which NF-κB is activated by the viral oncoproteins.