Infection of baby hamster kidney cells (BHK-21/13) with
Saint Louis encephalitis (SLE) virus depressed the rate of
protein and
ribonucleic acid (
RNA) synthesis until
viral RNA synthesis began 6 hr postinfection (PI). Virus-directed
RNA synthesis was subsequently inhibited until 12 hr PI when virion maturation began. The rate of
protein synthesis reached a peak 6 hr PI and was subsequently depressed until just before the onset of virion maturation. Density gradient analysis of
phenol-extracted
RNA from
actinomycin-treated infected cells indicated that, at 6 to 8 hr and again at 12 to 20 hr PI, three species of viral-specific
RNA were synthesized. The most rapid sedimenting form (43S) was
ribonuclease-sensitive and had a base composition similar to the
RNA isolated from mature virions. The 20S
RNA species was
ribonuclease-resistant and had a sedimentation coefficient and base composition similar to the replicative form associated with other
arbovirus infections. The 26S
RNA was
ribonuclease-resistant (0.2 mug/ml, 0.1 m NaCl, 25 C, 30 min) and had a
nucleotide base composition closer to the 20S form than to the values for 43S
RNA. Five-minute pulse labeling of infected cultures during the period
viral RNA synthesis was maximal resulted in labeling of only the 20S to 22S
RNA fractions. With pulse-labeling periods of 10 min, both the 20S and 26S
RNA species were radioactive. Periods of radioactive labeling of as long as 15 min were required before the 43S form was radioactively labeled. These results suggest that the 20S and 26S
RNA may be intermediate forms in the synthesis of 43S
viral RNA.