Immune co-stimulation and the Kaposi's virus

June 12, 2001

Viruses of the herpesvirus family have developed numerous innovative strategies to establish themselves in their host by evading, destroying, or redirecting host immune cells. Here, Coscoy and Ganem define a novel pathway through which the human herpesvirus associated with Kaposi's sarcoma (KSHV) acts on the B cells that it infects to block the protective response of cytotoxic T lymphocytes (CTLs). B cells are a major target of KSHV and are key to host defenses against the virus, because they act as antigen presenting cells (APCs) to activate CTL responses against infected cells. As is generally seen in APC-T cell interactions, efficient activation of CTLs against KSHV requires not just that the B cells present a viral peptide in an appropriate MHC context, but also that they express one or more co-stimulatory proteins. Coscoy and Ganem show that the viral protein K5 acts specifically the surface expression of two costimulatory proteins, ICAM and B7.2, causing them to be internalized rapidly and routed to the lysosome. In the absence of these proteins on the B cell surface, interacting T cells fail to induce the usual program of gene expression that is associated with active CTL responses. Because K5 resides in the ER protein of infected cells, its specific and profound effect on the fate of surface-expressed ICAM and B7.2 remains a puzzle.

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