Newborns are more susceptible to infections due to their lack of immunological memory and under-developed immune systems. Passive maternal immunity protects neonates until their immune systems have matured. We questioned if a noncytolytic virus that produces strong T cell responses in adults would also induce a response in neonates. Neonates were infected with LCMV at 5e4, 500, 50, 5 and 0.5 PFU. Surprisingly, at all doses the majority of pups succumbed to infection during the peak of the T cell response. Death was caused by T cell-dependent pathology and not viral load as 100% of T cell deficient pups survived with minimal lung and liver pathology. However, passive immunity from LCMV-immune mothers protected 100% of pups from death by helping control viral load early in infection. In adult mice high antigenic stimulation can cause over-activation of T cells leading to clonal exhaustion, where cells undergo a stepwise loss of function. Clonal exhaustion allows for survival from some high dose viral infections and results in persistent infection. We found that neonates without passive immunity that survived to day 14 did not show signs of T cell clonal exhaustion. Furthermore, surviving pups were not persistently infected, clearing virus by week 3. Neonates are commonly thought to have less functional immature immune systems, but these results show that neonates are capable of producing strong T cell responses that contribute to increased mortality.
- Copyright © 2013 by The American Association of Immunologists, Inc.