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* Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305;
Department of Pediatrics, Virginia Commonwealth University/Medical College of Virginia, Richmond, VA 23298;
BD Immunocytometry Systems, San Jose, CA 95131;
Biostatistics Division, Department of Health Research Policy, Stanford University, Stanford, CA 94305; and
¶ MedImmune, Mountain View, CA 94043
Healthy young children who acquire CMV have prolonged viral shedding into the urine and saliva, but whether this is attributable to limitations in viral-specific immune responses has not been explored. In this study, we found that otherwise immunocompetent young children after recent primary CMV infection accumulated markedly fewer CMV-specific CD4+ T cells that produced IFN-
than did adults. These differences in CD4+ T cell function persisted for more than 1 year after viral acquisition, and did not apply to CMV-specific IFN- production by CD8+ T cells. The IFN--producing CD4+ T cells of children or adults that were reactive with CMV Ags were mainly the CCR7low cell subset of memory (CD45R0highCD45RAlow) cells. The decreased IFN- response to CMV in children was selective, because their CCR7low memory CD4+ T cells and those of adults produced similar levels of this cytokine after stimulation with staphylococcal enterotoxin B superantigen. CD4+ T cells from children also had reduced CMV-specific IL-2 and CD154 (CD40 ligand) expression, suggesting an early blockade in the differentiation of viral-specific CD4+ T cells. Following CMV acquisition, children, but not adults, persistently shed virus in urine, and this was observable for at least 29 mo postinfection. Thus, CD4+ T cell-mediated immunity to CMV in humans is generated in an age-dependent manner, and may have a substantial role in controlling renal viral replication and urinary shedding.
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