The effect of progressive long term dietary protein depletion on viral susceptibility was investigated in 2 host-virus systems: (1) swine influenza in the male CF1 mouse, and (2) Rous sarcoma virus in the New Hampshire red chicken. Data are presented demonstrating a relationship between host protein nutrition and susceptibility to virus infection. This relationship is shown to be cyclic in character, involving phases of increased and decreased viral susceptibility. The relative resistance of the host on low protein intake is a function of the duration on incomplete diet administration before virus inoculation, and consequently a function of the host's state of depletion. As illustrated in Fig. 6, the cyclic susceptibility change demonstrated by these animals on low protein diet was characterized by an initial phase of increased susceptibility, a secondary phase of increased resistance, and a final phase of increased susceptibility. It is proposed that these alterations in relative viral susceptibility result from metabolic changes occurring within the host during the process of dietary protein depletion. The resistance changes are roughly correlated to periods of depot fat utilization (increased susceptibility), reserve protein utilization (decreased susceptibility), and tissue breakdown subsequent to protein starvation (increased susceptibility).

Many previously published concepts of the interplay of viral susceptibility and host nutrition maintained that host malnourishment led to increased host resistance. The cyclic change in resistance, reported herein, is given as evidence that the effect of host deficiency cannot be explained simply on the basis of an inhibition of virus growth due to retarded cellular metabolism in the host. Protein deficiency is shown not to produce an "all-or-none" effect, but a series of reproducible phases of increased and decreased resistance.

From the aforementioned results it is proposed that the phases of viral susceptibility seen in the protein-deficient host are demonstrative of the dynamic interrelationship between the physiologic state and the resistance of the host. Dietary influences in the normal host, by producing similar metabolic changes, could have analogous implications on innate resistance. It is believed that the foregoing leads to a more clear and dynamic concept of viral resistance in the normal individual.

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