Abstract

The isolation and physical mapping of a class of mutants designated large plaque (Ip) mutants of adenovirus (Ad) type 2 (group C) within the E1B 19 kDa- coding region provided initial clues about the functions of E1B 19-kDa protein (Chinnadurai et al. 1979; Chinnadurai 1983). A class of mutants designated the cytocidal (cyt) mutants of Ad12 (group A) isolated by Takemori and colleagues (Takemori et al. 1968) which also produce large plaques on infected cell monolayers was subsequently mapped to the E1B 19 kDa-coding region by intertypic mutant complementation (Subramanian et al. 1984b). The cyt mutants of Ad12 induce extensive cytopathic effect on infected cells (Takemori et al. 1968). As expected, subsequent studies revealed that several Ad2 and Ad5 mutants defective in the 19-kDa protein (19K mutants) also induced severe cytopathic effects (Subramanian et al. 1984b; Takemori et al. 1984). In accordance with an observation by Mak and colleagues (Ezoe et al. 1981 ) that viral DNA is extensively degraded in cells infected with Ad12 cyt mutants, several Ad2/Ad5 19K mutants were also found to induce fragmentation of cellular and viral DNA (deg) in infected cells (Subramanian et al. 1984a; Pilder et al. 1984; White et al. 1984a). Genetic studies have indicated that the cyt and deg phenotypes are linked, thereby indicating that the fragmentation of cellular and viral DNA is a consequence of the cytopathic effect induced by the 19K mutants (Subramanian and Chinnadurai 1986).

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