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A rapid disaggregation of host cell polyribosomes takes place after infection with picornavirus (5, 6) . Later, when virus-modified protein synthesis begins, larger polyribosomes appear in the cytoplasm of infected cells . Ribosomes in these new aggregates are linked by longer messenger RNA, in this case viral RNA molecules (2, 3, 6, 7, 9) and usually have a conventional arrangement (1) . Normal cells of the 37 RC line contain a fairly well-developed system of granular endoplasmic reticulum (GER) and free ribosomes organized in relatively small polysomes unpublished results) . After inoculation of these cells with poliovirus, the profiles of GER become distended and finally disappear . Concomitantly, the number of free ribosomes augments and larger polyribosomal aggregates are formed. An appreciable fraction of these aggregates has a typical form of helical polyribosomes . Data concerning the appearance of helical polyribosomes in poliovirus-infected 37 RC cells are presented in this note and discussed on the basis of the kinetics of virus growth and virus-dependent decline of protein synthesis. Throughout this study, confluent monolayers of 37 RC cells (Cercopithecus kidney cells ; G. Rita, personal communication) obtained in 30-m1 plastic Falcon Culture Flasks # 3012 were used (Falcon Plastics, Division of B-D Laboratories, Inc., Los Angeles, Calif.). The monolayers were propagated and maintained in Eagle's medium (MEM) supplemented with 10% inactivated calf serum. Poliovirus type I (Mahoney strain) was propagated in monkey kidney (MK) cells in MEM with 10 0/0 inactivated calf serum . Infected MK cells were collected 7 hr after inoculation, frozenthawed three times, and centrifuged . The suBRIEF NOTES

FORMATION OF HELICAL POLYRIBOSOMES IN POLIOVIRUS-INFECTED CELLS OF THE 37 RC LINE