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Biochemical Aspects of Leukemia Virus-induced Immunosuppression: Effect of Friend Disease Virus on Spleen Nucleases and Nucleic Acids¹

Departments of Microbiology, Albert Einstein Medical Center, Philadelphia, Pennsylvania 19141, and Temple University School of Medicine, Philadelphia, Pennsylvania 19140

The effect of Friend disease virus infection on spleen acid nuclease activity was studied in detail. RNase activity decreased rapidly, with time, during the course of the virus-induced leukemogenesis. Within 3 to 12 days after infection there was an 80 to 90% or greater suppression of RNase activity, as calculated per mg spleen tissue or protein. RNase activity remained depressed throughout the net period of 12 days. In contrast, DNase activity decreased sharply during the first 3 days after infection and then returned to near normal levels.

There was little or no change of total DNA content per mg protein spleen tissue in infected mice. However, RNA levels decreased moderately and then increased sharply during the 1st week of infection.

Studies on the subcellular distribution of nucleases and nucleic acids indicated that there was little, if any, detectable RNase in the nuclear, mitochondrial, and microsomal fraction of spleens of infected mice, as compared to the significant amounts of this enzyme in similar fractions of normal spleens. Most of the RNase activity in infected spleens was found only in the supernatant fraction.

There was little significant difference in the localization, distribution, and quantity of DNase activity in subcellular splenic fractions of normal or control animals. The only difference was the slight decrease in DNase activity in the nuclear and supernatant fractions in infected spleens.

Most of the RNA in the spleens of both infected and control animals was in the microsomal fractions. However, there was twice as much RNA in this fraction with infected spleens, as compared to controls. There was little or no significant difference in the DNA content of the various subcellular fractions of normal or infected animals.

¹ Supported in part by Research Grants GB 3228 and GB 6215 from the National Science Foundation and Grant T382 C from the American Cancer Society.

Received 5/29/69. Accepted 7/30/69.