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Updated: Jun 3, 2025

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
Published on: August 25, 2017
The Role of vIL-6 in KSHV-Mediated Immune Evasion and Tumorigenesis
Somayeh Komaki1, Tomoki Inagaki1, Ashish Kumar1
1Department of Dermatology, School of Medicine, University of California Davis, Sacramento, CA 95817, USA.
Abstract:
Kaposi's sarcoma-associated herpesvirus (KSHV) is a double-stranded DNA gamma herpesvirus. Like other herpesviruses, KSHV establishes a latent infection with limited gene expression, while KSHV occasionally undergoes the lytic replication phase, which produces KSHV progenies and infects neighboring cells. KSHV genome encodes 80+ open reading frames. One of the KSHV genes, K2, encodes viral interleukin 6 (vIL-6), a homolog of human IL-6 (hIL-6), mainly expressed in the lytic phase of the virus. vIL-6 plays a crucial role in regulating the expression of other viral genes and is also associated with inducing angiogenesis, cell survival, and immune evasion, which is suggested to promote the development of KSHV-associated diseases. This review summarizes the current knowledge on vIL-6. We focus on the vIL-6 regarding its protein structure, transcriptional regulation, cell signaling pathways, and contribution to the KSHV-associated diseases.
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