Abstract
Viral infection in the embryonated egg was controlled through appropriate temperature shifts. Through such control of the infection, certain groups of key tissues were implicated in the pathogenic processes that lead to death of the embryo, whereas other tissues were eliminated as relatively unimportant. Temperature shift-down experiments suggested that some mutants could resume the infectious process after relatively long periods (ribonucleic acid-negative mutants, Sts-4 and Sts-17) at the nonpermissive temperature, whereas others (RNA-positive mutants, Sts-2 and Sts-10) could not resume infection, even after a relatively short period at the nonpermissive temperature.
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Selected References
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