EFFECTS OF LARGE DOSES OF X-RAYS ON THE SUSCEPTIBILITY OF THE MONKEY TO EXPERIMENTAL POLIOMYELITIS.
In two series of the experiments here recorded the monkey which had been repeatedly exposed to x-rays responded with typical acute poliomyelitis to an intracerebral inoculation of poliomyelitic virus filtrate, whereas the normal control receiving the same dose showed no symptoms. In another series the x-rayed animal came down with typical poliomyelitis after inoculation with three-fourths of the dose which was not infective for the control. It has been demonstrated that the x-rays diminished both the number of circulating lymphocytes and the resistance of the animal to the weak poliomyelitic virus. Whether the lowered resistance of the animals as the result of the treatment with x-rays is due to the reduction of circulating lymphocytes in each of the x-rayed monkeys is not determined in these experiments. However, the great reduction in lymphocytes in human cases and in monkeys during the acute stage of experimental poliomyelitis and the gradual return of the cells to their former numbers during recovery strongly suggest a definite relation between these cells and one factor of resistance in poliomyelitis. On the other hand, the reduction in resistance by x-rays, while definite, is not sufficiently great to warrant the conclusion that we are dealing with major factors governing infection or non-infection. Another experiment in this paper deals with the survival of a subinfective dose of the virus in the normal monkey brain. A monkey receiving the subinfective dose of the virus was exposed to x-rays at 28 days, another at 15 days after injection, but neither animal showed symptoms of poliomyelitis. It is concluded that within this period the virus did not remain unchanged in the normal monkey brain. An attempt to reduce the immunity in a monkey acquired by an attack of experimental poliomyelitis was unsuccessful.
Amoss
H L
HL
Laboratories of The Rockefeller Institute for Medical Research.
Taylor
H D
HD
Witherbee
W D
WD