RESPONSE OF BHK21 CELLS TO INFECTION WITH TYPE-12 ADENOVIRUS .I. CELL KILLING AND T-ANTIGEN SYNTHESIS AS CORRELATED VIRAL GENOME FUNCTIONS

BHK21 cell killing by type 12 adenovirus (Ad12) has been shown (1) to be a viral genome function, (2) to require only one successfully infecting virus particle, and (3) to be induced with an efficiency somewhat greater than the initiation of viral early protein synthesis, measured as Ad12 tumor-specific antigen (T Ag). When the multiplicity of infection is increased beyond that required to initiate T Ag synthesis in 98% of the cells, a persistent surviving fraction of cells is found, the magnitude of which is dependent on the extent and rate of cell multiplication during the first 24 hours after infection. Analysis of T Ag synthesis in clones produced by infected cells indicates that while infected cells can divide initially, the capacity to synthesize T Ag is not replicated, since the multiplying cells are all T Ag (-) even though they may be the offspring or sisters of T Ag (+) cells. While single T Ag (+) cells may persist for several days after infection, most of these detach from the coverslip within 24-48 hours after infection and can no longer give rise to clones. The increased survival of cells infected at high multiplicity while in logarithmic growth cannot be accounted for only by dilution of the infecting genomes and is not due to a genetically resistant cell type in the population. © 1969.