Protection of the villus epithelial cells of the small intestine from rotavirus infection does not require immunoglobulin A

Immunoglobulin A (IgA) is the primary immune response induced in the intest ine by rotavirus infection, but vaccination with virus like particles induc es predominantly Igc, not IgA, To definitively assess the role of IgA in pr otection from rotavirus infection, IgA knockout mice, which are devoid of s erum and secretory IgA, were infected and then rechallenged with murine rot avirus at either 6 weeks or 10 months. Following primary rotavirus infectio n, IgA knockout mice cleared virus as effectively as IgA normal control mic e. Rotavirus-infected IgA knockout mice produced no serum or fecal IgA but did have high levels of antirotavirus serum Ige and IgM and fecal Igc, wher eas IgA normal control mice made both serum IgA and Ige and fecal IgA, Both IgA normal and IgA knockout mice were totally protected from rotavirus cha llenge at 42 days. Ten months following a primary infection, both IgA norma l and knockout mice still had high levels of serum and fecal antirotavirus antibody and were totally protected from rotavirus challenge, To determine if compensatory mechanisms other than IgG were responsible for protection f rom rotavirus infection in IgA knockout mice, mice were depleted of CD4(+) T cells or CD8(+) T cells. No changes in the level of protection were seen in depleted mice, These data show that fecal or systemic IgA is not essenti al for protection from rotavirus infection and suggest that in the absence of IgA, Ige may play a significant role in protection from mucosal pathogen s.