Tumor-inducing properties of the mammary tumor agent in young and adult mice.
The mammary tumor-inducing activity of the mammary tumor agent was studied by the administration of either one or five injections of fractions of transplanted mammary cancer into mice ranging in age from 22 to 126 days.

The concentration of the fractions represented the amount of the agent derived from either 2 × 10-2 or 10-3 gm. equivalents of fresh tissue.

In general, the incidences observed in adult mice could not be correlated with the amount of the agent that was injected.

The highest incidence occurred in the progeny of the mice which received a single injection of the fraction with the lowest concentration of the agent.

The transmission of the agent was observed following the administration of the mammary tumor agent into both young and adult females.

No significant difference was to be seen in the transmission of the agent in the milk of either cancerous or noncancerous experimental mice.

Data were presented suggesting that the age resistance to the tumor-inducing action of the mammary tumor agent may be determined, in part, by the genetic constitution of the test animals. Other possibilities were discussed.
Lack of Resistance of Adult Mice to Erythrocyte-borne Bittner Virus
BITTNER virus, the classical mouse mammary tumour virus (MTV), can be detected in bioassays of various organs and tissues of infected mice including mammary tissues and erythrocytes1–3. We have shown that the final result of the administration of MTV-carrying RBC or of mammary tissue extracts to young hosts is identical: namely, the production in test mice which are free from MTV of mammary nodules and tumours containing electron microscopically visible B particles. The MTV in these two tissues differ, however, in several respects2,3. MTV activity in mammary tissues (M-MTV) is itself associated with B particles, but such particles do not seem to be associated with RBC which bear MTV activity (R-MTV). Resistance to tumorigenesis of adult animals following oncogenic viral administration is well known4. Several investigators have demonstrated that adult mice are more resistant than young ones to mammary tumour development after administration of MTV5,6. We have recently suggested that this resistance in adult mice of the BALB/c strain is systemically mediated7. Dux and Mühlbock8, however, have proposed that both host age and tissue age are involved in the resistance of older mice to MTV. R-MTV has been shown to precede the appearance of M-MTV in naturally infected mice3, and so it was thought possible that a failure in R-MTV production which followed administration of M-MTV to adult mice might account for the low incidence of mammary nodules and tumours. We have now compared the effects of administration of the two forms of MTV to mice of different ages.
Immune dysfunction following infection with chicken anemia agent and infectious bursal disease virus. II. Alterations of in vitro lymphoproliferation and in vivo immune responses.
To determine the functional impact of alterations in lymphocyte concentrations and ratios following infection with chicken anemia agent (CAA) alone or in combination with infectious bursal disease virus (IBDV) on the immune system of young chickens, in vitro lymphoproliferation assays and in vivo responses to vaccination with several common viral agents were assessed at various time intervals post-inoculation (PI). Concanavalin A (Con A), phytohemagglutinin (PHA) and pokeweed mitogen (PWM) stimulation of splenic lymphocytes (SPL) collected from control birds could not be detected until 10-14 days PI. Infection with CAA was characterized by significantly higher PWM stimulation of SPL at 17 days PI and significantly lower PWM stimulation of peripheral blood lymphocytes (PBL) at 14 days PI, compared with uninfected controls. Concanavalin A and PWM stimulation of SPL was significantly increased in birds inoculated with IBDV alone. Lymphocytes harvested from birds inoculated simultaneously with CAA and IBDV had significantly lower responses. Effects on humoral and cell-mediated immunity following CAA and/or IBDV were determined by evaluating vaccination responses to Newcastle disease virus (NDV), fowl pox virus (FPV) and infectious laryngotracheitis virus (ILTV) during the acute phase of CAA infection (2 weeks PI). Vaccination of birds 2 weeks following CAA infection at 1 day of age resulted in decreased protection against NDV (85.7%) and ILTV (7.1%) challenge compared with protection rates in control birds (100% and 53.3% respectively). Infectious bursal disease virus infection was associated with decreased protection against NDV (60%) only. Concomitant infection at 1 day of age resulted in a greater reduction in NDV challenge protection (33.3%), slightly decreased FPV protection (87.5%), increased numbers of persistent FPV vaccination lesions and increased protection against ILTV challenge (71.4%). Vaccination of birds 2 weeks following CAA infection at 2 weeks of age resulted in slightly decreased NDV humoral antibody, development of persistent FPV vaccination lesions (17%) and increased immunity to ILTV challenge compared with control birds (83.3% vs. 66.7%). Chickens inoculated with IBDV alone displayed a more severe depression in NDV antibody titers and only a slight decrease in ILTV protection. Vaccination following concomitant infection at 2 weeks of age resulted in a higher percentage of FPV persistent vaccination lesions (39%) and greatly enhanced immunity to ILTV challenge (100%).