Open AccessInfluence of Input Multiplicity of Infection on the Antiviral Activity of Interferon
Author(s) -
Lothar Stitz,
Huub Schellekens
Publication year - 1980
Publication title -
journal of general virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.55
H-Index - 167
eISSN - 1465-2099
pISSN - 0022-1317
DOI - 10.1099/0022-1317-46-1-205
Subject(s) - interferon , vesicular stomatitis virus , vaccinia , biology , virology , virus , multiplicity of infection , vesicular stomatitis indiana virus , recombinant dna , genetics , gene
The antiviral activity of interferon was shown to be dependent on the input m.o.i. Cells could not be protected against the cytopathogenic effect of vaccinia, herpes, Echo or vesicular stomatitis virus at m.o.i. greater than 1. At a m.o.i. of less than or equal to 1, cells could be protected but the amount of interferon necessary to yield protection was inversely related to the m.o.i. When protection was afforded, it was only transient. The duration of the antiviral effect of interferon was also inversely related to the m.o.i. The dependence of the antiviral effect on the m.o.i. could not be explained by assuming the viruses to be mixtures of subtypes with different interferon sensitivity. Also, selection by interferon treatment of interferon-insensitive subtypes could not be shown. The greater antiviral effect of interferon at low m.o.i. was probably not caused by induction of interferon by the infecting virus. A direct inactivation by the virus of the antiviral effect of interferon could not be demonstrated. These results indicate that when interferon-treated cells are infected, they will not survive the infection. The only result of the interferon treatment will be to inhibit virus replication to some extent, leading only to a delay in cell death.