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*
Partners AIDS Research Center and
Massachusetts General Hospital Cancer Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129; and
Universitaets Spital Zurich, University of Zurich, Zurich, Switzerland
Kaposi’s sarcoma-associated herpes virus (KSHV) is a recently
identified human 
2-herpesvirus associated with Kaposi’s sarcoma,
primary effusion lymphoma, and Castleman’s disease. We reasoned that
CTL responses may provide host defense against this virus, and
consequently, KSHV may have evolved strategies to evade the
CTL-mediated immune surveillance. In this study six B cell lines
latently infected with KSHV were found to express reduced levels of HLA
class I surface molecules compared with B cell lines transformed by the
related -herpesvirus EBV. KSHV-infected cells also required higher
concentrations of soluble peptides to induce efficient CTL-mediated
lysis than control cell lines and were unable to process and/or present
intracellularly expressed Ag. Incubation of the KSHV-infected cell
lines with high concentrations of soluble HLA class I binding peptides
did not restore the deficient HLA class I surface expression. To assess
the underlying mechanisms of these phenomena, TAP-1 and TAP-2 gene
expression was analyzed. While no attenuation in TAP-2 expression was
observed, TAP-1 expression was significantly reduced in all KSHV cell
lines compared with that in controls. These results indicate that KSHV
can modulate HLA class I-restricted Ag presentation to CTL, which may
allow latently infected cells to escape CTL recognition and persist in
the infected host.
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