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Evidence is accumulating that replication of animal viruses may take place in naturally resistant cells provided measures are taken to circumvent the barrier to infection presented at the cell surface and thus to place the virus directly in contact with the biosynthetic factory of the cell. The only technique by which this has so far been accomplished consists in exposing resistant cells to viral nucleic acid (NA), which, unlike complete infectious particles, attains, under appropriate conditions, an intracellular position. Holland and his associates' presented the first example of the capacity of viral NA to initiate infection in resistant cells when they showed that poliovirus RNA induced in chick embryonic cells replication of complete virus. That cells even very distantly related to those of the natural host may also support virus replication when exposed to viral NA was subsequently demonstrated in three reports of 1964.2-4 These findings are significant from the point of view of general biology, since they support the concept of the universality of the genetic code. They also have practical implications, since they suggest the possibility that populations of cells which can be easily and economically propagated in large quantities and which are naturally resistant to certain agents such as poliovirus might be employed in the mass production of vaccine or as a means of isolating and growing agents of diseases like infectious hepatitis which so far have defied all attempts at cultivation. But for such purposes the requirement imposed by the necessity of using viral NA renders direct application of the method impractical. We have therefore considered how it might be possible to introduce complete virus into resistant cells under conditions that permit cell survival. A simple way of doing this was suggested by recent demonstrations that certain myxoviruses when added in high concentration to cell suspensions rapidly bring about fusion of the cytoplasm of the individual elements, which results in the formation of viable multinucleate cells (for summary of literature see ref. 5). We speculated that if such fusion is brought about in the presence of complete virions, those which by chance are in contact with the cell surfaces where coalescence occurs might be incorporated within the cytoplasm of the polynucleate complex. To explore the possibility that virus could in this manner be placed within cells considered to be resistant and there might replicate, we selected, as virus, Poliovirus I and, as cell systems, secondary chick embryo cells and an established line of hamster embryo cells. We adopted Sendai virus, which Harris and his associates6 have applied in their studies of artificial heterokaryons, as the fusion-inducing agent.

REPLICATION OF POLIOVIRUS I IN CHICK EMBRYO AND HAMSTER CELLS EXPOSED TO SENDAI VIRUS