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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
Published on: September 14, 2010
Kaposi's Sarcoma-Associated Herpesvirus Latency Locus Compensates for Interleukin-6 in Initial B Cell Activation
Sang-Hoon Sin1, Sun Ah Kang2, Yongbaek Kim3
1Department of Microbiology and Immunology, Program in Global Oncology, Lineberger Comprehensive Cancer Center, and Center for AIDS Research, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA sang-hoon_sin@med.unc.edu.
Abstract:
Interleukin 6 (IL-6) is considered a proliferation and survival factor for B cells. To assess the role of IL-6 in Kaposi sarcoma-associated herpesvirus (KSHV) latency, KSHV latency locus-transgenic mice (referred to as latency mice) lacking IL-6 were evaluated. IL-6(-/-) latency mice had the same phenotypes as the latency mice, i.e., increased frequency of marginal zone B cells, hyperplasia, and hyperglobulinemia, indicating that the KSHV latency locus, which includes all viral microRNAs (miRNAs), can compensate for lack of IL-6 in premalignant B cell activation.
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