Effects of Specific Antisera on the Growth of Bacterial Viruses (Bacteriophages).

When a suspension of bacterial viruses is mixed with specific antiserum, the virus particles are rapidly "inactivated," that is, they lose the power to attack bacteria and to multiply. This inactivation is due to the union of the virus particles with the antibody. The union is irreversible but does not destroy the virus. The original virus may be recovered if the antibody is digested with papain (Kalmanson and Bronfenbrenner, 1943). Why does the union of the virus with the antibody inactivate the virus? Does it merely prevent adsorption of the virus on the bacterial host cell or does it block a later step in the process of virus growth? Hershey (private communication) has found that virus which is barely inactivated (by exposure to antiserum for a short time or at a high dilution) is still adsorbed by the bacteria. Under these conditions the antibody must interfere with a later step of virus growth. In the present paper we wish to report experiments which attack these problems by somewhat different methods. In previous work (Burnet, Keogh, and Lush, 1937; Hershey, 1943; Hershey, Kalmanson, and Bronfenbrenner, 1943) the serum effects were tested by determining differences in the number or *ize of plaques formed by a virus suspension after various treatments. In our experiments we determined also the latent period of virus growth and the yield of virus from infected bacteria. In the previous study, moreover, treatment of the virus suspension with antiserum always preceded the adsorption of virus on its host. We were interested to find out whether any effect of the antibody on the virus could be detected if the antibody was added to virus already adsorbed on bacteria. In this paper we also wish to report experiments with antibacterial sera. Such sera are always totally inactive against viruses which can attack the bacteria, that is, when antibacterial serum is mixed with virus and incubated, subsequent titrations of the virus show no reduction of the plaque count. However, very striking effects are obtained when the bacteria are treated with antibacterial serum prior to the addition of the virus. The virus growth may then be completely or partially inhibited. These experiments were begun for the purpose of using the antisera in a study of interference between different viruses simultaneously attacking the same host. The interference experiments will be reported in a subsequent paper. The preliminary experiments constitute, howeve'r, an independent attack on the general problem of the mechanism of growth of bacterial viruses. Our experi-