Respiratory infection of young infants results in increased morbidity and mortality compared to infection of adults. In spite of the significance of this health issue, our understanding of the immune response elicited in infants especially in the respiratory tract is highly limited. We developed a nonhuman primate model to probe the virus-specific antibody response in infants following infection with influenza virus. Infection of infants resulted in more pulmonary damage and higher viral loads compared to adults. While the systemic IgG antibody response was similar in infant and adult animals, the response in the upper respiratory tract of the infant was compromised. This lower response was associated with an increased prevalence of Treg cells and low levels of BALT. These data suggest a defect in the ability to produce effective virus-specific antibody responses at the local infection site is a contributor to increased pulmonary damage in the at-risk infant population.