The mechanism of virus attachment to host cells. IV. Physicochemical studies on virus and cell surface groups

Abstract

1. 1. Study of the effects of a variety of group-specific and nonspecific reagents on the attachment reaction of T2 bacteriophage to its host cell have been carried out. Loss of the cell's ability to bind T2 virus occurs only through the action of reagents which block its carboxyl groups. Loss of the virus' ability to attach to the cell occurs only through the action of reagents which block the virus amino groups. 2. 2. These results, together with earlier physicochemical studies on the electrostatic nature of the attachment reaction, permit the conclusion that positively charged amino groups on T2 virus bond to complementarily situated carboxyls on the cell surface. 3. 3. T1 virus also appears to bind to its host by amino and carboxyl links, but with this virus the possibility exists that both types of groups from each body may be involved in the attachment. 4. 4. The failure of Tl or T2 bacteriophages to agglutinate host cells indicates that the virus attachment organ is a singular site on the surface, and hence supports the results of electron-micrographie studies which indicate that the tail is the attachment organ. 5. 5. A nonspecific and noninvasive cell attachment of both bacteriophages has been demonstrated to occur in the presence of high concentrations of H +. T2 virus also exhibits nonspecific cell binding in the presence of other strongly binding cations and in excessive concentrations of polyphosphate. The absence of the characteristic ability to discriminate between resistant and sensitive cells indicates that the chemical groups responsible for the nonspecific reaction are not identical to those responsible for normal attachment. 6. 6. A large variety of reagents tested failed to split the T2 virus into its deoxyribonucleic acid and protein moieties. Hence, the assumption is strengthened that the splitting which occurs even at low temperatures at the surface of a negatively charged resin is specific and, hence, probably similar to that which occurs in the course of normal invasion at the surface of a negatively charged host cell.