AKTivation of PI3K/AKT/mTOR signaling pathway by KSHV

被引：110
作者：
Bhatt, Aadra P. [1 ,2 ]
Damania, Blossom [1 ,2 ]
机构：
[1] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA
[2] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA
来源：
FRONTIERS IN IMMUNOLOGY | 2013年 / 3卷
关键词：
Akt; KSHV; mTOR; PI3K; B cells; SARCOMA-ASSOCIATED-HERPESVIRUS; PROTEIN-COUPLED-RECEPTOR; PRIMARY EFFUSION LYMPHOMA; NF-KAPPA-B; MULTICENTRIC CASTLEMANS-DISEASE; PRIMARY ENDOTHELIAL-CELLS; FOCAL ADHESION KINASE; RIBOSOMAL S6 KINASE; KAPOSIS-SARCOMA; NUCLEAR ANTIGEN;
D O I：
10.3389/fimmu.2012.00401
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
As an obligate intracellular parasite, Kaposi sarcoma-associated herpesvirus (KSHV) relies on the host cell machinery to meet its needs for survival, viral replication, production, and dissemination of progeny virions. KSHV is a gammaherpesvirus that is associated with three different malignancies: Kaposi sarcoma (KS), and two B cell lymphoproliferative disorders, primary effusion lymphoma (PEL) and multicentric Castleman's disease. KSHV viral proteins modulate the cellular phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway, which is a ubiquitous pathway that also controls B lymphocyte proliferation and development. We review the mechanisms by which KSHV manipulates the PI3K/AKT/mTOR pathway, with a specific focus on B cells.
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页数：16
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