Introduction. Following the discovery of interference in influenza infections by incomplete forms of the virus (von Magnus, 1951), Cooper & Bellett (1959) found a similar phenomenon in vesicular stomatitis virus (VSV) infections, and showed that it was due to transmissible components, defective interfering (DI) particles (Hackett, 1964; Huang & Wagner, 1966), which are usually generated when VSV is passaged at a high multiplicity of infection (m.o.i.). DI particles can replicate only during co-infection with standard or non-defective (ND) helper virus, and in such mixed virus infections the replication of the helper virus is greatly repressed. Bellett & Cooper (1959) observed a reciprocal exponential relationship between the m.o.i. of DI particles in the inoculum and the yield of infectious virion progeny, and deduced that co-infection of a cell with a single DI particle is sufficient to repress the helper virus in one passage (compare Sekellick & Marcus, 1980). DI particles enjoy a replicative advantage over ND virions, and once generated they quickly become the dominant viral species during high m.o.i. passage.


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