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Blood, 15 October 2001, Vol. 98, No. 8, pp. 2474-2481
IMMUNOBIOLOGY
Human herpesvirus 7 induces the functional up-regulation of
tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)
coupled to TRAIL-R1 down-modulation in CD4+ T
cells
Paola Secchiero,
Prisco Mirandola,
Davide Zella,
Claudio Celeghini,
Arianna Gonelli,
Marco Vitale,
Silvano Capitani, and
Giorgio Zauli
From the Department of Morphology and Embryology, Human
Anatomy Section, University of Ferrara; the Department of
Biomorphology, G. D'Annunzio University of Chieti; the Institute of
Human Anatomy, University of Parma, Italy; and the Institute of Human
Virology, University of Maryland Biotechnology Institute, Baltimore.
Human herpesvirus 7 (HHV-7) is endemic in the adult human
population. Although HHV-7 preferentially infects activated
CD4+ T lymphocytes, the consequence of T-cell infection for
viral pathogenesis and immunity are still largely unknown. HHV-7
infection induces apoptosis mostly in uninfected bystander cells but
not in productively infected CD4+ T cells. To dissect the
underlying molecular events, the role of death-inducing ligands
belonging to the tumor necrosis factor (TNF) cytokine superfamily was
investigated. HHV-7 selectively up-regulated the expression of
TNF-related apoptosis-inducing ligand (TRAIL), but not that of CD95
ligand or TNF- in lymphoblastoid (SupT1) or primary activated
CD4+ T cells. Moreover, in a cell-to-cell-contact assay,
HHV-7-infected CD4+ T lymphocytes were cytotoxic for
bystander uninfected CD4+ T cells through the TRAIL
pathway. By contrast, HHV-7 infection caused a marked decrease of
surface TRAIL-R1, but not of TRAIL-R2, CD95, TNF-R1, or TNF-R2. Of
note, the down-regulation of TRAIL-R1 selectively occurred in cells
coexpressing HHV-7 antigens that became resistant to TRAIL-mediated
cytotoxicity. These findings suggest that the TRAIL-mediated induction
of T-cell death may represent an important immune evasion mechanism of
HHV-7, helping the virus to persist in the host organism throughout its lifetime.
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