Induction of a new enzyme in rabbit kidney cells by pseudorabies virus

Role of Herpes simplex Virus Thymidine Kinase Expression in Viral Pathogenesis and Latency

“…In 1963, the induction of thymidine kinase (TK) enzyme activity in herpes simplex virus (HSV)-infected cells was reported by Kit and Dubbs [1], and similar results were reported in pseudorabies virus-infected cells by Nohara and Kaplan [2], The latter publication was the first to report that the TK activity induced by the herpesvirus infection was vi rus specific [2], and within several years, it was evident that HSV expressed viral-speci fic TK activity [3][4][5][6]. Over the ensuing years, TK genes and TK enzyme activity were de scribed for many herpesviruses (table 1), as well as other DNA viruses [27,28]; and, it is expected that viral-specific TK activity will be reported for other viruses, including other herpesviruses.…”

Kinetics of Synthesis of Various Types of Antigenic Proteins in Cells Infected with Pseudorabies Virus

“…The identity and function of all of these p)roteins has not been ascertained, but presumably these "early" proteins include a variety of virus-induced enzymes which are essential for the synthesis of viral components. Infection of RK cells with PR virus also induees an increase in the activity of enzymes involved in the synthesis of DNA, and there are indications that some of these enzymes differ from those performing the same function in normal, noninfected cells (Nohara and Kaplan, 1963). These enzymes may thus be antigenically different from those found in normal cells and may constitute at least part of the IE antigens.…”

“…For example, the synthesis of cellular DNA is arrested and only viral DNA is synthesized in these infected cells (Kaplan and Ben-Porat, 1963). An increase in the level of activity of a number of enzymes involved in the synthesis of deoxyribonucleic acid (l)NA), some of which appear to differ in their physical properties from those performing the same function in noninfected cells, is also observed in PR virus-infected cells (Nohara and Kaplan, 1963).…”

Incorporation of 5‐bromodeoxyuridine and 5‐iododeoxyuridine Into Viral Dna and Its Effect on the Infective Process*

“…The fact that in IUDR-treated cells viral DNA and viral antigen do accumulate but are assembled only to a small extent into viral particles posed the following questions: Is most of the IUDR-containing viral DNA incapable of being coated by viral protein: i.e., does the presence of the iodine atom so alter the structure of viral DNA that it cannot fit into the viral coat, or is the lack of assembly due to the production in the IUDR-treated cells of proteins involved in the process of virus assembly that are defective in their normal function? To differentiate between these two possibilities, we made use of the fact that viral DNA forms within the cell a precursor pool from which DNA is withdrawn at random for the integration into mature virus particles (Ben-Porat & Kaplan, 1963). Thus, if the reason for the inability of IUDR-containing viral DNA to become integrated into viral particles is due to the formation of abnormal proteins, the synthesis of which is controlled by IUDR-DNA, it should be possible to obtain integration of this DNA into viral particles by allowing the cells to synthesize normal viral DNA before or after the period of synthesis of IUDR-DNA.…”

“…--39 10 THE EFFECT OF IUDR AND BUDR ON THE REGULATION OF ENZYME ACTIVITY Infection of RK cells in the stationary phase of growth with Pr virus leads to a large increase in the activity of some of the enzymes involved in the synthesis of DNA (Nohara & Kaplan, 1963). Since the substitution of thymidine by IUDR appears to be responsible for the synthesis of what most likely are faulty proteins involved in the assembly of virus particles, it was of interest to determine whether the incorporation of IUDR and BUDR into progeny viral DNA also affects the mechanisms controlling the level of activity of these enzymes in the cell.…”