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Journal of Virology, November 2006, p. 10874-10878, Vol. 80, No. 21
0022-538X/06/$08.00+0 doi:10.1128/JVI.00767-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231
Received 14 April 2006/ Accepted 18 August 2006
Human
herpesvirus 8 (HHV-8) viral interleukin-6 (vIL-6) mediates signaling
through the gp130 signal transducer but unlike human IL-6 (hIL-6) does
not require the nonsignaling gp80
subunit of the IL-6
receptor complex. By utilizing a gp80-refractory vIL-6 variant,
vIL-6(R189L), we found that signal transduction, as measured by STAT1
and STAT3 activation and gp130 tyrosine phosphorylation in
gp80+/gp130+ HEK293T cells, was
modulated by gp80. Furthermore, the signaling and BAF-130 cell
growth-promoting activities of vIL-6 and hIL-6 could be distinguished,
and exogenous addition of soluble gp80 enhanced cell growth supported
by vIL-6. Our findings demonstrate that gp80 can modulate vIL-6
activity and that vIL-6 and hIL-6 signaling are not directly
equivalent.
Published
ahead of print on 6 September 2006.
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