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SUMMARYInfection of a cowpea line by cowpea severe mosaic virus (CPSMV) was inhibited by cowpea mosaic virus (CPMV) even though the plants were immune to CPMV. The inhibition was dose-dependent and was complete if CPMV was added to the inoculum in a 50-fold excess over CPSMV. Isolated CPMV RNA inhibited infection by CPSMV or by isolated CPSMV RNA. CPMV particles devoid of RNA (top component), u.v.-inactivated but intact CPMV particles or u.v.-inactivated CPMV RNA did not inhibit infection by CPSMV. Bottom component particles of CPMV, but not middle component particles, inhibited CPSMV to the same extent as unfractionated CPMV. These findings strongly suggest that the interference is not due to competition between the particles or the RNAs of the two viruses for infectible sites. It may be that CPMV infects cells of the 'immune' host subliminally and that the inhibition is associated with replication of at least bottom component RNA of CPMV.

During an infection with cowpea mosaic virus (CPMV) both virion assembly and formation of tubules associated with plasmodesmata are required for cell-to-cell movement. These functions are encoded by the M-RNA of CPMV. To study the mechanism of CPMV movement, mutant N123 was used in complementation studies with sunn-hemp mosaic virus (SHMV), a legume-infecting tobamovirus. Previous studies have shown that N123 fails to spread in cowpea plants because of mutation(s) in its M-RNA. However, the mutant was efficiently replicated in cowpea protoplasts, in which virions were formed and tubular transport structures were induced. After high-dose inoculation of cowpeas with N123, only a few infected protoplasts could be isolated, indicating that cell-to-cell transport of N123 was greatly impaired, if not completely abolished. Upon coinoculation with SHMV, mutant N123 infected cowpea plants systemically and accumulated to levels which were comparable to those of wild-type CPMV. In contrast, separate B-RNA of CPMV and a CPMV deletion mutant lacking the tubule-inducing function, were complemented by SHMV to only low levels. It is concluded that SHMV-facilitated spread of CPMV in the non-virion tobamovirus mode is inefficient and that spread of mutant N123 is probably in the CPMV mode, SHMV providing an as yet unidentified helper function.