Modulation of nuclear factor-kappaB by human T cell leukemia virus type 1 Tax protein: implications for oncogenesis and inflammation.
Activation of the nuclear factor kappa B (NF-kappaB) transcription factor family by different stimuli, such as inflammatory cytokines, stress inducers, or pathogens, results in innate and adaptive immunity. While the main function of NF-kappaB is to promote the host's immune response, the NF-kappaB pathway is frequently dysregulated by invading viral pathogens. Human T cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL) and an inflammatory disease named tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). HTLV-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses. Here, we review current thinking on how Tax may affect both diseases through activation of NF-kappaB signaling.
Peloponese
Jean-Marie
JM
Molecular Virology Section, Laboratory of Molecular Microbiology National Institute of Allergy and Infectious Diseases, National Institutes of Health Bethesda, Maryland 20892-0460, USA.
Yeung
Man Lung
ML
Jeang
Kuan-Teh
KT
D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000276:immunology*; D016356:Gene Products, tax / Q000276:immunology*; D015490:HTLV-I Infections / Q000276:immunology*; D015368:Human T-lymphotropic virus 1 / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D016328:NF-kappa B / Q000276:immunology*
D016356:Gene Products, tax; D016328:NF-kappa B