• 1 January 1980
    • journal article
    • research article
    • Vol. 44 (4), 433-439
Abstract
The role of trypsin in plaque production by simian rotavirus SA-11 in monolayers of [rhesus monkey kidney] MA-104 cells was investigated. Initial trypsin treatment of the virus alone or its presence only during the early phases of virus-cell interaction was insufficient for plaque production by the virus. Presence of trypsin (5 .mu.g/ml) in the agar overlay throughout the 5 day incubation period was essential for the optimal development of the virus plaques. Production of plaques by the incorporation of trypsin in the overlay was not due to the enzymatic degradation of any plaque-inhibitors in the agar used. Experiments using high (4 PFU[plaque-forming units]/cell) and low (35 PFU/106 cells) multiplicities of infection suggest that trypsin added to fluid maintenance medium facilitates the cell-to-cell spread of progeny virus particles. The enzyme incorporated in the agar overlay appears to play a similar role, thereby assisting in the formation of SA-11 plaques.