Summary
The virus yields and number of infectious centres of HSV infected mouse neuroblastoma C1300 cells (clone 41 A3) infected at different multiplicities of infection (MOI) were found to vary more than the differences of HSV concentrations of the virus suspensions used for infection of the cells. This suggested that a C1300 cell had to be infected with more than one HSV particle in order to produce progeny virus—multiplicity activation. The greater than expected enhancement of virus production of C1300 cell cultures receiving increasing MOI of HSV was probably not due to improved virus adsorption, nor influenced by non-virus factors in the virus inoculum stimulatory for HSV replication. A hypothesis, that the block in virus replication was promoted by an inhibitor of an HSV specified regulatory protein and could be overcome by the addition of HSV DNA copies in the infected cell, was supported by the results of two types of experiments. Presence of phosphonoformic acid, an inhibitor of the HSV specified DNA polymerase, in the culture medium of HSV infected permissive GMK cells resulted in non-linear relationships between virus yields and MOI. An HSV temperature sensitive mutant (ts B5), defective in a late structural protein, rescued wild type HSV in C1300 cells.
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Vahlne, A., Nilheden, E. & Svennerholm, B. Multiplicity activation of herpes simplex virus in mouse neuroblastoma (C1300) cells. Archives of Virology 70, 345–356 (1981). https://doi.org/10.1007/BF01320249
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DOI: https://doi.org/10.1007/BF01320249