The primary antibody response to alumadsorbed BSA was depressed when initiated during low-grade chronic Plasmodium berghei malaria in mice, as previously reported during acute P.y. yoelii infection. Induction of immunological memory by soluble polymerized BSA was abolished in both infections; in infected hosts this normally immunogenic stimulus resulted in partial tolerance. In contrast to the depression of immune response, neither infection interfered with the induction of low-zone tolerance by monomeric BSA. The rate of non-immune elimination of BSA was found to be normal during acute malaria, and only slightly reduced in chronic infection. These results may be explained in terms of abnormal antigen handling in infected mice, due to some functional defect in macrophages, although this does not seem to be a sufficient explanation for all the phenomena of malaria-associated immunosuppression.