Abstract
Summary: The drug 5-iodo, 2-desoxyuridine (IDU) does not prevent adsorption of herpesvirus to cells but does prevent virus replication. Treatment of cells with the drug immediately after infection results in a loss of 96 to 99.5% of the input virus infectivity. Most of this loss occurs during the eclipse and the very early growth periods. The progeny of the surviving 0.5 to 4.5% fraction of virus is more resistant to similar destruction by IDU treatment. IDU stops viral replication already under way in infected cells but does not inactivate infectious virus already formed within these cells. IDU is unable to prevent or reverse significantly the cytopathic effects of herpesvirus on tissue culture cells. In fact, a highly reproducible cytotoxic effect is observable in infected cells in which viral replication is completely arrested by IDU treatment. When this cytotoxic effect was quantitated by counting the numbers of affected cells it was found to be about half of the infectious unit concentration. This cytotoxic characteristic is three times more stable to ultraviolet irradiation than is the infectivity and, thus, appears to be distinguishable from infectivity. Herpesvirus within infected cells is quite stable to thermal inactivation in the presence or absence of IDU; therefore, eradication of virus already present in tissue cultures solely by use of this drug would require long periods of time.

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