Vitamin A deficiency results in multiple derangements that impair the
response to infection, This review focuses on experimental models of s
pecific virus infections and on cytokines and cells with cytolytic act
ivity important to antiviral defenses, Altered specific antibody respo
nses and greater epithelial damage in vitamin A-deficient hosts are co
nsistent findings, The cytolytic activity of natural killer cells and
various cytokine responses are altered, The inflammatory response to i
nfection may also result in derangements in the transport and metaboli
sm of retinol, We speculate that interaction of several factors may co
mbine to explain the greater severity of infection seen in vitamin A-d
eficient animals and children, In addition to a preexisting lack of ti
ssue vitamin A, these factors may include reduced mobilization and inc
reased excretion of retinol during the acute phase response to infecti
on, poor innate and specific immune response to virus, and delayed rep
air of damaged epithelia. Foci of vitamin A-deficient epithelia may be
sites of penetration of bacteria and other agents, leading to seconda
ry infections and contributing to an increased severity of infections
and poor outcome in vitamin A-deficient animals and humans.