In mouse L cells infected with vesicular stomatitis virus (VSV), the synthesis of 45 S rRNA and its conversion to 28 S and 18 S rRNA are inhibited during the course of infection. Evidence is presented that the lack of accumulation of stable rRNA species results not only from the decreased transcription and processing of 45 S rRNA, but also from an increased breakdown of pre-rRNA or stable rRNA during processing. In cells prelabeled with [3H]uridine and then infected, the 28 S and 18 S rRNA species remain unaffected. Studies using uv-irradiated VSV indicate that the viral function involved in rRNA synthesis inhibition is slightly more sensitive to uv irradiation than the function involved in processing inhibition. These results suggest that the VSV functions involved in 45 S rRNA synthesis and processing inhibition may be related, or overlapping, but not identical. In cells infected by VSV mutant T1026R1, total RNA synthesis is inhibited, but the distribution of precursor and stable rRNA species remains nearly normal for up to 5 hr after infection. The function of the mutant virus involved in the inhibition of rRNA processing appears to be defective. In mengovirus-infected L cells, 45 S rRNA synthesis, but not processing, is severely inhibited soon after infection, indicating that a decrease in rRNA transcription is not necessarily accompanied by a decrease in processing.