Kaposi's Sarcoma-Associated Herpesvirus Latency Locus Compensates for Interleukin-6 in Initial B Cell Activation.

Authors:
Sang-Hoon Sin
Sang-Hoon Sin
Dept. Microbiology & Immunology / University of North Carolina at Chapel Hill
Research Assistant Professor
KSHV
Chapel Hill, NC | United States

J Virol 2016 02 9;90(4):2150-4. Epub 2015 Dec 9.

Department 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.

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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Source
http://dx.doi.org/10.1128/JVI.02456-15DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4734016PMC
February 2016
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