The KSHV viral interleukin-6 is not essential for latency or lytic replication in BJAB cells.
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.
Chen
Lei
L
Department of Microbiology, University of Washington, 1959 N.E. Pacific Street, Box 357242, Seattle, WA 98195, USA.
Lagunoff
Michael
M
D000818:Animals; D045744:Cell Line, Tumor; D002522:Chlorocebus aethiops; D004279:DNA, Viral / Q000235:genetics; D019288:Herpesvirus 8, Human / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism*; D010957:Plasmids / Q000235:genetics; D014709:Vero Cells; D017735:Virus Latency / Q000502:physiology*; D014779:Virus Replication / Q000502:physiology*
D004279:DNA, Viral; D015850:Interleukin-6