This project focuses on the immunology, immunoprophylaxis, and microbiology of acute intestinal infections: viral, bacterial and parasitic.  Antigens associated with gut flora appear to cause clonal expansion of antigen-sensitive cells of appropriate specificities in Peyer's patches and also drive the process of B-cell differentiation such that cells in Peyer's patches preferentially become committed to expression of IgA antibodies.  Techniques for studying "cross-priming" of mucosal surfaces by respiratory and enteric antigens have been developed.  Protein deficiency has been shown to markedly impair a specific mucosal immune response to a protein antigen.  The migrating patterns of IgA memory cells, antigen-specific suppressor cells and cells destined to produce specific IgA antibody after enteric immunization with cholera toxin have been partly determined.  Cells conveying memory and suppression disseminate to distant mucosal surfaces whereas IgA plasmablasts home largely to the organ of origin.  The DNA sequences for E. coli LT A- and B-subunits have been cloned separately and the recombinant plasmids are available for study.  Efforts are underway to develop a more reliable adult animal model for toxigenic E. coli diarrhea so that E. coli strains which produce defective LT can be studied as possible live vaccines.  Detailed studies of the viral nucleic acids and proteins of the SA-ll and porcine rotaviruses are underway.  Progress has been made in purification of the structural polypeptides of SA-ll; the rates of synthesis of these and non-structural polypeptides in infected cells have been studied; a serodiagnostic facility to support clinical and epidemiologic studies of human rotavirus infections has been established.