Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. STKE, 19 November 2002
Vol. 2002, Issue 159, p. tw433
[DOI: 10.1126/stke.2002.159.tw433]

EDITORS' CHOICE

VIROLOGY Viral Pusher, Cell Junkie

Kaposi's sarcoma herpesvirus (KSHV) causes B cell lymphomas as well as blood-filled skin tumors in which the virus multiplies along with the tumor cells. Virus infections induce the host to produce interferon-{alpha}, a mediator of innate immune responses. Chatterjee et al. show that interferon-{alpha} stimulates the KSHV-infected cells to produce a mimic of a host cytokine, interleukin 6. The host's IL-6 binds to two cell surface receptors, gp80 and gp130, but viral IL-6 needs only gp130 to signal the cell. During other virus infections, interferon-{alpha} inhibits gp80 expression, preventing IL-6 binding, dooming the infected cells to death by apoptosis, and contributing to clearing the host of infection. By contrast, KSHV IL-6 continues to signal the cell via gp130 alone, effectively immortalizing the cell, and allowing it and the virus to proliferate together.

M. Chatterjee, J. Osborne, G. Bestetti, Y. Chang, P. S. Moore, Viral IL-6-induced cell proliferation and immune evasion of interferon activity. Science 298, 1432-1435 (2002). [Abstract] [Full Text]

Citation: Viral Pusher, Cell Junkie. Sci. STKE 2002, tw433 (2002).



To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882