On observation by scanning electron microscopy, the respective diameters of heat-induced gel networks ofmyosin B and soybean protein CIF were found to be above 1 /mi and below 1 /mi. In a mixture of the proteins, it was observed that the denatured soybean protein CIF had associated continuously around myosin B networks. These reactions reinforced the rough myosin B networks. The structures of the reinforced networks were considerably different from those of the individual proteins. Furthermore, when both the proteins were mixed, formation of the networks was already found before heating. It was suggested that the reaction was related to disulfide bonds between the two proteins.

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Recently, we reported that heat-killed Lactobacillus casei (LC) protected mice from murine cytomegalovirus (MCMV) infection by augmentation of natural killer (NK) cell activity. In the present study, we examined which components of LC cell induce the nonspecific resistance most effectively. Whole cell preparation of original LC, susceptible to bacteriophages SG-T and J1, was more effective than its mutants resistant to either bacteriophage. Although the activity of LC cells decreased upon fractionation, cell wall fractions were more active than cytoplasmic fractions. Glycoprotein (GP), a cell wall constituent, was a potent inducer of the resistance. The relative activity of cellular components to induce the resistance was evaluated by a protection index, a ratio of plaque-forming units (PFU) per 50% lethal dose (LD50) for treated mice to that for untreated mice. The protection indices of LC cells and GP were approximately 80 and 28, respectively. The protective effect of GP was evidenced by a decrease in titers of infectious viruses replicated in the target organs. Not only LC cells but also GP, although to a lesser degree, enhanced NK cell activity both in uninfected mice and MCMV-infected mice. The activity of LC cells and GP to augment NK cell activity correlated with the protection index. GP treatment did not modify interferon (IFN) production during MCMV infection. Thus, GP of LC cells seems to be the active principle to endow mice with resistance to MCMV.

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