The occurrence of both minor and gross mutational changes in the genomes of poxviruses has been linked with alterations in host range or in the disease manifested in either the natural or laboratory setting. The effects of such mutations on the infectious processes are amenable to careful analyses, using procedures to evaluate a variety of phenotypic markers, such as the degree of virulence, thermosensitivity, pock or plaque type, serological relatedness, capacity for complementation or recombination, host restriction and defectiveness in virus specified metabolic processes or virion assembly. New techniques of exquisite sensitivity, utilizing restriction endonucleases, “Southern-transfer” (Cooper and Moss, 1978), and R-loop mapping make it possible to pinpoint individual mutations due even to single base alterations (McFadden et al., 1980, Schümperli et al., 1980) and to identify the outcome of such mutations by characterizing changes in single polypeptides by means of O’Farrell’s two-dimensional PAGE (Essani and Dales, 1979; McFadden et al., 1980). In the case of the orthopoxviruses, studies to date reveal that spontaneous mutations can frequently arise in the form of deletions which may be relatively minor, involving fewer than 250 base pairs (McFadden and Dales, 1979), or deletions can be more extensive, encompassing a loss of several thousand bases (Archard and Mackett, 1979; Moyer and Rother, 1980). Both types of excision occur in the vicinity of the terminal crosslinks in the genome and involve the inverted terminal repetition sequences (De Filippes, 1976; Mackett and Archard, 1979; Wittek et al., 1978a; Garon et al., 1978).
KeywordsVaccinia Virus Myxoma Virus Variola Virus Chick Embryo Fibroblast Inverted Terminal Repetition Sequence
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