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J. Virol. doi:10.1128/JVI.00062-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Protracted course of LCMV-WE infection in early life: induction but limited expansion of CD8⁺ effector T cells and absence of memory CD8⁺ T cells

World Health Organization Collaborating Center for Vaccinology and Neonatal Immunology, Departments of Pathology-Immunology and Pediatrics, University of Geneva, Geneva, Switzerland

^* To whom correspondence should be addressed. Email: claire-anne.siegrist{at}medecine.unige.ch.

	Abstract

Viral infections in human infants frequently follow a protracted course, with higher viral loads and delayed viral clearance. To identify the mechanisms responsible for this protracted pattern of infection, we developed an infant infection murine model using the well-characterized LCMV-WE strain in 2-week-old BALB/c mice. In contrast to adult mice, in which viral clearance occurred as expected 8 days after infection, LCMV viral titers persisted for several weeks after infant infection. LCMV-specific effector CD8⁺ T cells were elicited in infant mice and fully functional on day 7, but rapidly waned and could not be recovered from day 12 onwards. We show here that this results from the failure of expansion of LCMV-specific CD8⁺ T cells and into the absence of protective LCMV-specific memory CD8⁺ T cells. Under these early life conditions, viral control and clearance are only eventually achieved through LCMV-specific B cells that contribute to protect infant mice from early death or chronic infection.