No evidence was found to support the idea that vaccine virus placed in the cisterna magna is capable of producing an acute disseminated encephalomyelitis with perivascular demyelination either in normal or in partially immune monkeys. A testicular extract (Reynals' factor) did not induce vaccine virus to cause an acute disseminated encephalomyelitis in monkeys. Repeated intramuscular injections of brain extracts and brain emulsions into eight monkeys were followed in two instances by an inflammatory reaction, accompanied by demyelination, in the central nervous system. The exact relation of the injections to the disease of the nervous system is not clear. The combined action of vaccine virus and an emulsion of fresh rabbit brain did not lead to the production of an acute disseminated encephalomyelitis in monkeys that had received repeated intramuscular injections of emulsions and alcohol-ether extracts of normal rabbit brains.
Experiments are reported in which it is shown that if rabbits are deprived of food, the lesions resulting from injection of vaccinia are either fewer or smaller; presumably this is partially explainable on reduction of available nutrients in the cell. The number and character of the lesions are also modified by the state of hydration of the interstitial tissues: If the amount of interstitial fluid is increased by permitting the animal to drink water, the lesions are even less numerous; but if the interstitial tissues are dehydrated either by withholding water or by injecting physiological saline solution into the peritoneal cavity, then the lesions are more numerous. The increase in interstitial fluids in these experiments was not due to decreased plasma proteins, for these were normal. In this respect, therefore, the rabbit differs from man, for unless the plasma proteins are reduced, simple starvation in man results in dehydration rather than edema of the tissues. From these experiments it is concluded that the virus is less able to multiply in the poorly nourished cell than in the well nourished one, and that hydration of the tissues increases the resistance of the tissue to infection while dehydration has the opposite effect. It is suggested that this is because hydration tends to localize the virus in situ, with result that fewer cells are exposed to it, while dehydration has the opposite effect. However, actual changes in cell susceptibility consequent upon altered water balance may be responsible for the effect.
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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