Infection of mice with lactic dehydrogenase virus (LDV) resulted in a lifelong elevation of a number of plasma enzymes including lactic dehydrogenase, isocitric dehydrogenase, malic dehydrogenase, phosphohexose isomerase, and glutamic-oxaloacetic transaminase (1). Recent studies on the mechanism of enzyme elevation showed that infected mice cleared endogenous enzymes at a slower rate than uninfected mice (1). The present study was undertaken to see whether the catabolism of a "nonenzymatic" protein, T-globulin, was also altered. The experiments reported herein show that the catabolism of intlavenously administered I m ~'-globulin was not impaired in virus-infected mice, but that the level of endogenous 3,-globulin was elevated, and that the capacity of the infected mouse to produce antibody to a heterologous protein (human ~'-globulin) was enhanced. Materials and MethodsAnimals.--Except where indicated otherwise, conventional CAF-1 male mice, 4 to 6 wk old, obtained from the animal production section of the National Institutes of Health (NIH) were used throughout these experiments. Germfree male and female mice, 3 to 4 wk old, of the NIH stock colony were supplied by Dr. C. E. Miller of the Germfree Unit, Laboratory Aids Branch, and were housed in plastic isolators (2) in the Gnotobiotic Section of the National Institute of Dental Research. All materials introduced into the plastic isolators were treated so as to eliminate viable bacteria. To check for contamination, urine and feces were cultured twice a week.Virus.--The method of preparation and the assay for LDV have been described previously (3). Stock pools P-16 and P-17 were used throughout these experiments. The titer of the pools was approximately 10 l°.°IDs0/ml and all dilutions were made in Eagle's basal medium or 0.85% sodium chloride (saline). Mice were infected routinely with LDV by injecting intra-* Present address:

A variety of viable and non-viable bacteria became mineralized with hydroxyapatite when implanted in dialysis bags in the peritoneal cavities of rats. The microscopic pattern of mineral deposition appeared analogous to that in the formation of oral calculus. Since nonviable organisms were mineralized at an accelerated rate, bacterial metabolic processes may not be essential for mineralization.

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