Abstract
A viral genome codes for only part of the genetic information necessary for its self-replication. The host contributes the machinery for energy production, the building blocks of viral nucleic acids and proteins, and a transcription-translation apparatus. Despite the universality of the genetic code and of basic metabolic pathways, however, a wild-type viral genome that succeeds in invading a given, normally metabolizing host cell may possibly not yield progeny: for normal virus growth, the viral genome apparently has to be in tune with the genome of the host in regard to factors that are highly specific for a given virus. In addition to examples of such situations in animal virology (Dulbecco, 1969; Bang, 1972), several phage-bacteria systems are known in which virus infection is abortive, or results in a low yield of progeny virus. In phage genetics, the most extensively investigated mechanism of abortive infection by wild-type viruses is that of DNA restriction: the injected viral DNA is cut to pieces by the action of nucleotide sequence-specific restriction enzymes of the host (see review: Meselson et al., 1972). The physical destruction of the invading phage genome is an efficient, straightforward way of interfering with the normal course of viral development. However, several other examples of abortive infection by wild-type phages are known, in which interference with the physical integrity of the invading genome does not seem to be the cause for failure of phage growth (Hausmann et al., 1968; Morrison and Malamy, 1971; Georgopoulos, 1971; Moyer et al., 1972). In such cases, at what stages of viral development and by which mechanisms does the block occur?
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