Abstract

When turnip, sugar beet, or spinach seedlings were grown for varying periods in soils containing tomato black ring (TBRV) and raspberry ringspot viruses, and then transplanted to virus-free soil, some seedlings became infected in 3 days and many in 9 days. The ease with which TBRV infected and multiplied in roots decreased with increasing age of seedling. The presence of the viruses in soils was shown by growing bait seedlings in them, but not by inoculating leaves of test plants with soil extracts. In highly infective soils, one bait seedling became infected per 100-200 g soil. Infectivity of soils was abolished by air drying for a week at 20°C and was decreased by freezing at minus 10°C. It was also abolished by treating soils with pentachloro-nitrobenzene, tetramethylthiuram disulfide, ethylene dibromide, and Nemagon, but not by griseofulvin or by mixing the soil with lime or ammonium sulfate. Infectivity of soils containing TBRV was associated with particles that sedimented through 7 cm water in between 30 seconds and 5 minutes, and to a lesser extent with particles sedimenting in 30 seconds.
Pot experiments showed that seedlings grown in noninfective field soil or autoclaved soil did not become infected when watered with highly infective sap. TBRV became established in autoclaved sand when watered with crude eelworm preparations from infective soils, but not when the sand was mixed with washed roots of naturally infected plants. TBRV also became established in noninfective field soil when it was cropped with artificially infected sugar beet. The receptivity of this soil to virus seemed specific to the beet ringspot strain of tomato black ring virus and was abolished by autoclaving. Evidence is adduced that an agent occurring in soil plays a part in transmission of TBRV, and its possible identity among soil-inhabiting organisms is discussed.