Antiviral activity (AVA) determined by the inhibition of the cytopathic effect (CPE) of vesicular stomatitis virus (VSV) on mice fibroblasts, was measured in the peritoneal effluent of mice. Four groups of animals (each group numbering 30 mice) were studied. Group 1 consisted of sham operated mice and served as the control group. Group 2 underwent implantation of silastic matter (of which the Tenckhoff catheter is made). In group 3, chronic renal failure was induced. Group 4 comprised those mice in which both chronic renal failure was induced and silastic matter implanted. Optical density readings, directly related to the inhibition of CPE were 0.66 +/- 0.01, 0.59 +/- 0.08, 0.85 +/- 0.06 and 0.86 +/- 0.13 for groups 1, 2, 3 and 4, respectively (p < 0.01 for groups 1 and 2 versus 3 and 4). Virus control readings indicative of the CPE of VSV without the presence of peritoneal effluent were 0.58 +/- 0.07, not significantly different from those obtained in groups 1 and 2. They were, however, significantly below values from groups 3 and 4 (p < 0.05). These data show that AVA is undetectable in the peritoneal effluent of normal mice. Chronic renal failure produces an enhancement of AVA. Silastic matter (Tenckhoff catheter) implantation does not play a role in the production of AVA.

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