HEN a pure bacterial culture is. attacked by a bacterial virus, the cul-W ture will clear after a few hours due to destruction of the sensitive ceIls by the virus. However, after further incubation for a few hours, or sometimes days, the culture will often become turbid again, due to the growth of a bacterial variant which is resistant to the action of the virus. This variant can be isolated and freed from the virus and will in many cases retain its resistance to the action of the virus even if subcultured through many generations in the absence of the virus. While the sensitive strain adsorbed the virus readily, the resistant variant will generally not show any affinity to it. The resistant bacterial variants appear readily in cultures grown from a single cell. They were, therefore, certainly not present when the culture was started. Their resistance is generally rather specific. It does not extend to viruses that are found to differ by other criteria from the strain in whose presence the resistant culture developed. The variant may differ from the original strain in morphological or metabolic characteristics, or in serological type or in colony type. Most often, however, no such correlated changes are apparent, and the variant may be distinguished from the original strain only by its resistance to the inciting strain of virus. The nature of these variants and the manner in which they originate have been discussed by many authors, and numerous attempts have been made to correlate the phenomenon with other instances of bacterial variation. The net effect of the addition of virus consists of the appearance of a variant strain, characterized by a new stable character-namely, resistance to the inciting virus. The situation has often been expressed by saying that bacterial viruses are powerful “dissociating agents.” While this expression summarizes adequately the net effect, it must not be taken to imply anything about the mechanism by which the result is brought about. A moment’s reflection will show that there are greatly differing mechanisms which might produce the same end result.

D’HERELLE (1926) and many other investigators believed that the virus by direct action induced the resistant variants. GRATIA (1921), BURNET (I929), and others, on the other hand, believed that the resistant bacterial variants are produced by mutation in the culture prior to the addition of virus. The