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J. Exp. Med.,
Volume 188, Number 6, September 21, 1998 1047-1054
By
,*,*,*
in,
,*
From the * Department of Histology and Embryology, and the Reactivation from latent cytomegalovirus (CMV) infection is often associated with conditions
of immunosuppression and can result in fatal disease. Whether the maintenance of systemic
CMV latency is mainly governed by factors of the infected cell or by immune control functions
is unknown. Likewise, the putative immune control mechanisms which could prevent the induction and spread of recurrent CMV infection are not clearly identified. We took advantage
of latently infected B cell-deficient mice and a sensitive method for virus detection to study
CMV reactivation after ablation of lymphocyte subsets. A crucial role of both T lymphocytes
and natural killer (NK) cells was demonstrated. Within 5 d after depletion of lymphocytes, productive infection occurred in 50% of mice, and 14 d later 100% of mice exhibited recurrent infection. A hierarchy of immune control functions of CD8+, NK, and CD4+ cells was established. Reactivation was rare if only one of the lymphocyte subsets was depleted, but was
evident after removal of a further subset, indicating a functional redundancy of control mechanisms. The salivary glands were identified as the site of most rapid virus shedding, followed by
the detection of recurrent virus in the lungs, and eventually in the spleen. Our findings document a previously unknown propensity of latent CMV genomes to enter productive infection
immediately and with a high frequency after immune cell depletion. The data indicate that
only the sustained cellular immune control prevents CMV replication and restricts the viral genome to a systemic state of latency.
Department of Physiology and
Immunology, Faculty of Medicine, University of Rijeka, 51000 Rijeka, Croatia; and the § Max von
Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Lehrstuhl Virologie,
Ludwig-Maximilians-Universität, München, D-80336 München, Germany
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