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J. Exp. Med.,
Volume 187, Number 12, June 15, 1998 1941-1951
By
From the Department of Veterinary Pathology, The University of Edinburgh, Edinburgh EH9 1QH,
United Kingdom
It is currently believed that latently infected, resting B lymphocytes are central to gammaherpesvirus persistence, whereas mucosal epithelial cells are considered nonessential. We have readdressed the question of nonlymphoid persistence using murine gammaherpesvirus 68 (MHV-68). To dissect lymphoid from nonlymphoid persistence, we used µMT transgenic mice that
are defective in B cells. MHV-68 DNA persisted in the lungs of intact and B cell-deficient mice. Both episomal and linear forms of the virus genome were present in lungs, implying the
presence of both latency and productive replication. In situ hybridization for virus tRNA transcripts revealed latent MHV-68 in pulmonary epithelial cells. Infectious virus was recovered
from the lungs of µMT mice after T cell depletion, showing that the persisting virus DNA was
reactivatable. Finally, using adoptive transfer of B cells into B cell-deficient mice, it was shown
that virus persisting in lungs seeded splenic B cells, and virus resident in the spleen seeded the
lungs. These results show that mucosal epithelia can act as a nonlymphoid reservoir for gammaherpesvirus persistence, and that there is a two-way movement of virus between lymphoid and
nonlymphoid compartments during persistence.
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