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Updated: Jul 19, 2026

Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus
Published on: August 15, 2025
The KSHV viral interleukin-6 is not essential for latency or lytic replication in BJAB cells
1Department of Microbiology, University of Washington, 1959 N.E. Pacific Street, Box 357242, Seattle, WA 98195, USA.
Abstract:
Kaposi's Sarcoma-associated herpesvirus encodes a homolog of the human cellular interleukin-6 that may play a formative role in many KSHV-related diseases. While the viral IL-6 can signal similarly to its human counterpart little is known about the role of vIL-6 during KSHV infection. Using homologous recombination and selection in eukaryotic cells, a KSHV isolate was purified that does not express vIL-6 as was a control recombinant that left vIL-6 intact. The two viruses establish and maintain latency to similar levels in BJAB B-cells, reactivate to similar levels in B-cells and Monkey kidney cells and have very similar KSHV gene expression patterns. BJAB cells expressing KSHV survive better than the parental BJAB cells in low serum and the vIL-6 deletion does not abrogate this growth advantage. Thus vIL-6 is not essential for establishment, maintenance, or reactivation from latency in cell culture and is not involved in the survival of infected BJAB B-cells in low serum.
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