INFECTIOUS BOVINE RHINOTRACHEITIS VIRUS REPLICATION, CYTOPATHOLOGY, AND PLAQUE FORMATION IN THE PRESENCE AND ABSENCE OF NUCLEIC ACID ANALOGUES.

Stevens, Jack G. (University of Washington, Seattle), and Neal B. Groman. Infectious bovine rhinotracheitis virus replication, cytopathology, and plaque formation in the presence and absence of nucleic acid analogues. J. Bacteriol. 87:446-453. 1964.-Cytopathology induced by infectious bovine rhinotracheitis (IBR) virus was correlated with the one-step growth cycle. Nuclear alterations, including the development of inclusion bodies, preceded the appearance of virus. It was found that similar effects occurred in the presence of 5-bromodeoxyuridine (BUDR) and 5-fluorodeoxyuridine (FUDR), compounds which depress the yield of "standard" virus from a range of 116 to 500 to less than 0.5 plaque-forming units per cell. As with known members of the herpesvirus group, IBR virus plaques developed and enlarged indefinitely in the presence of specific antibody. An analysis of the mechanism operative in this process was undertaken. The evidence suggested that neither viral nor subviral particles capable of replicating "standard" virus passed between cells during the first 8 hr of infection. This is the time preceding the release of extracellular virus from initially infected cells. With BUDR and FUDR, it was shown that plaques also developed in this system in the virtual absence of production of "standard" infectious virus. However, a class of analogue-dependent virus was found which may have been at least partly responsible for plaque formation in the analogue-treated system. The relative contributions of subviral particles or of a self-sustaining molecular disorganization to the process have not been completely assessed as yet.