SUMMARYHerpes simplex type I Angelotti (HSV-I ANG) virions were shown to contain two major acid-soluble proteins, BP~ and 2, which by size and charge analysis were also found to be associated with chromatin isolated from HSV-I ANG-infected African green monkey kidney cells (HSV-chromatin). BPI and z proved to exist in a phosphorylated state both in virions and in HSV-chromatin. BP~ consisted of a single polypeptide of 38 K tool. wt. which was correlated to the tegument protein VP22. In SDS-polyacrylamide gels BP2 migrated as a single polypeptide band with an apparent tool. wt. of iz K. Urea gel analysis revealed that BPz consisted of three components, BPza, b and c, of different phosphate contents. Arguments were provided that these components probably represent different polypeptides of similar mol. wt. HSV-chromatin, in addition to BPI, BP2a, b and c contained a further major virus-induced basic phosphopolypeptide of tool. wt. 65 K which was not detected in acid-extracts of mature virions.

A defective genotype of herpes simplex virus strain Angelotti (HSV ANG) accumulates in the course of controlled serial high MOI virus passages representing 50–60% of the total number of mature virions in the seventh of these passages. Defective HSV ANG significantly differs from other defective HSV genotypes described so far: the DNA of the defective particles has the same buoyant density as nondefective DNA. In contrast to non-defective HSV ANG DNA, it is not attacked by the restriction endonucleases Eco R I, Hpa I and Hind III. Defective virions strongly suppress the formation of progeny virus. They do not interfere, however, with the synthesis of HSV-specified thymidine (TdR) kinase.

During serial passages of Herpes simplex virus (HSV) at high multiplicity of infection, virions containing defective viral DNA accumulate in the progeny. The defective DNA molecules are made up by repeats of restricted portions of the standard viral genome. Two different classes of defective DNA derived from HSV-1 Angelotti (ANG) in independent series of high MOI-passages were studied. The nucleotide sequences contained in the defective DNA were localized on the parental viral genome. One of the two classes contained sequences from non-contiguous sites mapping in unique and in redundant regions of the parental DNA, whereas the second class apparently originates from the S-terminal redundant region of the parental DNA. The localization of defective DNA sequences was complicated by the fact that there exists sequence homology between the S-terminal redundancy and various unique DNA sequences in the L-segment of the HSV-1 ANG genome.