Virus-strain interference in relation to symptoms of psorosis disease of citrus

The citrus diseases described in literature as psorosis “A,” psorosis “B,” concave gum, blind pocket, crinkly leaf, and infectious variegation have been assumed to be caused by related virus strains because they all have the same characteristic symptom on young leaves. All are bud-perpetuated and graft-transmissible but are not known to be transmitted to any extent by other means. On psorosis A trees grown from infected buds, the scaling bark lesions develop after the trees are six or more years of age.

In studies of lesion initiation and symptom expression in relation to source of inoculum, young sweet orange trees infected by means of bark patches taken from non-lesion parts of psorosis A trees showed only the transitory young-leaf symptoms for a period of years. At later times typical, localized lesions of the psorosis A type developed on the inoculated plants. On the other hand, if inoculations result from bark taken directly from a lesion, the test trees react quickly. They show young-leaf symptoms, and bark symptoms begin to arise generally on the trees within three months. Later the mature leaves show rings and blotches, and small twigs die.

Sweet orange trees previously infected with psorosis A from non-lesion sources of inoculum showed no such immediate effects when reinoculated from psorosis A lesion sources. This protective reaction provided a means of testing the relationship of the psorosis virus strains. Trees first inoculated and systemically infected with the viruses of psorosis B, concave gum, blind pocket, crinkly leaf, and infectious variegation were protected as described above when reinoculated from psorosis A lesion bark. This demonstrated virus strain relationship. The quick decline (tristeza) virus provided no protection against psorosis.

Although trees reinoculated as described above are protected to the extent that they do not develop the early, severe symptoms, localized, slowly developing bark lesions develop after a year or more around the sites where the lesion bark inoculum used for reinoculation is introduced. The development of such lesions on trees invaded by virus from the previous inoculation from non-lesion inoculum more or less parallels the occurrence of lesions on orchard trees which normally develop in later years in spite of the fact that the virus has been present at all times. The spontaneous development of lesions on orchard trees and how they are initiated are not fully understood.

From the studies reported in this paper a hypothesis is advanced that psorosis A infected sweet orange trees carry two virus strains or components, one of which (component a) is capable of producing bark lesions and the other (component b) is not capable of producing lesions. In non-lesions bark, component a is the dominant part of the mixture and prevents component b from increasing sufficiently to bring about the injury that leads to lesion development. Bark lesions are initiated when component b by chance invades one or more plant cells ahead of component a. In the absence of a, component b increases in concentration and can then invade adjacent tissues and overcome the defense offered by the former. Such a procedure would explain the delayed appearance and slow enlargement of spontaneously developing lesions on orchard trees which have been systemically invaded by psorosis virus for many years. Some experimental evidence is presented to support this hypothesis.