CF # 1 germfree (GF) and conventional (CV) mice as well as offspring of conventionalized GF (GF-CV) mice were orally inoculated with Escherichia coli 0115a, c : K (B), a causative agent of megaenteron in mice. Although CV and GF mice showed no clinical signs and survived, all of the GF-CV mice died with diarrhea by day 14 after inoculation. Thickened wall of the large intestine, microscopically showing proliferation of crypt type cells, was seen in GF and GF-CV mice but not in CV mice. In addition, in GF-CV mice, hemorrhage and severe erosion with marked inflammatory reactions were observed. While the inoculated E. coli could not colonize in CV mice, a level of 10⁸ cells/g feces was maintained in GF mice from day 1 after inoculation to the end of examination (on day 28) and in GF-CV mice from day 5 to the time of death. Newly prepared germfree (GF-CV-GF) mice obtained hysterectomy from GF-CV mice showed a low sensitivity as comparable to that in GF mice. On the other hand, ex-germfree mice produced by oral administration of feces of GF-CV mice showed severe infection as comparable to that seen in GF-CV mice. These results suggest that the intestinal flora may play roles both on protecting from the infection of pathogenicE.. coli and on enhancing the infection.

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In vitro production of endotoxin-induced interferon in rabbit tissue cell cultures could be enhanced by pretreatment with interferon. The enhancible state developed from the first hr of incubation at 37 C and a maximal priming effect was attained at 6 hr of incubation. Yields of interferon from unprimed cultures were usually 20-200 units/ml. In contrast, the primed cultures constantly yielded 1, 000-2, 500 units/ml of interferon. The pretreatment with interferon seemed to cause an earlier appearance of detectable interferon and the primed cells became more sensitive to endotoxin.
It turned out that 10-30 units/ml of rabbit interferon were enough to develop the maximal priming. Even when cells were pretreated with higher doses of rabbit interferon such as 1.0 × 10⁴-1.0 × 10⁵ units/ml, the same level of priming effect was always observed without diminution. Various types of homologous (rabbit) and heterologous (human and mouse) interferon preparations showed similar dosedependent enhancement of interferon production in proportion to the antiviral titers of these preparations as tested with RK-13 cells of rabbit origin.

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For attempt to detect an etiological agent, cultures from bovine lymphosarcoma cases (adult form (ALS), calf form (CLS), and thymic form (TLS)) were maintained in vitro for over a 18 month period. In two cultures from ALS, bovine leukemia virus (BLV) antigen was constantly detected. On the other hand, BLV antigen remained negative in cultures from two CLS and one TLS cases up to 40 passages. The RNA dependent DNA polymerase activities in these cultures were also negative.
Treatment of a culture from CLS (3178) originated from liver tumor with 5'-iodo-2'-deoxyuridine (IdU) and dexamethasone (DXM) resulted in production of an agent serologically and morphologically similar to BLV and in alteration of cell morphology. No virus was detected in culture from TLS after treatment with IdU and DXM.

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Murine cytomegalovirus was utilized as a model for human cytomegalovirus, which had no experimental animal, to study immunoprophylaxis of the cytomegalovirus infections.
(1) Murine cytomegalovirus (MCMV) serially propagated in mouse embryonic fibroblasts had lost pathogenicity for weanling mice including neonatally thymectomized mice.
(2) The cell culture-adapted MCMV was effective as a “live, attenuated virus vaccine” against challenge by virulent, mouse-passaged MCMV.
(3) The immunization via intraperitoneal route protected mice from every parameter of MCMV infection. These included clinical signs, virus replication, histopathology and mortality.
(4) The protective immunity was active against the virulent MCMV which was not neutralized by the rabbit anti-attenuated MCMV serum.

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Transfer factor (TF) causes nonimmune lymphocytes to produce leukocyte migration inhibitory factor (LMIF) in the presence of purified protein derivative (PPD). The activity of TF was measured by leukocyte migration inhibitory test (LMIT). The LMIT was a modification of the conventional agarose droplet method. To express the activity of LMIF quantitatively and simply, LMIF titer was introduced. The LMIF titer was obtained from the combination of two factors, LMIF dilution and cell migration diameter, and therefore this made the LMIT much more sensitive as compared to the conventional LMIT. The responsiveness of lymphocytes from acute lymphoblastic leukemia (ALL) and from cell-mediated immunodeficiency in children to TF was assayed by LMIT. In ALL, the lymphocyte responsiveness was poor in relapse but improved with remission. The responsiveness was remarkably well in 3 patients with cell-mediated immunodeficiency. This method appears useful for the In Vitro evaluation of responsiveness of lymphocytes to TF.

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The concentrations of immunoglobulins and protein in piglet feces at one day to ten weeks of age were assayed by the single radial immunodiffusion and by the Lowry method, respectively.
The concentrations of IgG, IgA, IgM and total immunoglobulin were found to be significantly higher at one day and two days of age than those at one week to ten weeks of age. The concentrations of IgA, IgM and total immunoglobulin at two days of age were the highest and those at one day of age were the next highest. However, in case of IgG, there seemed to be no such difference in concentrations.
There was almost no significant difference in concentrations of IgG, IgA and total immunoglobulin in feces at one week to ten weeks of age. On the other hand, the concentration of IgM at eight weeks of age seemed to be the least from one day to ten weeks of age.
The concentration of protein at two days of age was the highest and that at one day of age was the next highest. Those at one week to three weeks of age were the least among those at one day to ten weeks of age.

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Erythematous delayed reactions without induration, presumably assigned to Jones-Mote type, were characterized by the resistance to treatment with cyclophosphamide (CY) before elicitation or immunization in guinea pigs immunized with BGG in IFA or CFA. CY-treatment before elicitation converted delayed erythematous reactions from negative to positive at late intervals after immunization with BGG in IFA. Such a treatment augmented erythematous delayed reactions in animals immunized with BGG in CFA, but abolished induration at the reaction sites. CY-treatment before elicitation or immunization reduced the numbers of basophils at the reaction sites, although erythematous delayed reactions were augmented. Effector T cells responsible for delayed erythematous reaction without induration appear to persist for a long period of time after immunization in the presence of antibody production or tuberculin hypersensitivity and the expression of their function may be inhibited by suppressive mechanisms.

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