Viroids and conventional plant viruses induce a very similar range of macroscopic symptoms (and presumably metabolic changes) in their hosts. Symptom expression is usually optimal at the same relatively high temperatures that promote viroid replication (i.e. 30-33°C). Prominent among metabolic changes are dramatic alterations in growth regulator levels. Stunting and leaf epinasty (a downward curling of the leaf lamina resulting from unbalanced growth within the various cell layers) are often considered the classic symptoms of viroid infection, and other commonly observed symptoms include vein clearing, veinal discoloration or necrosis, and the appearance of localized chlorotic/necrotic spots or mottling in the foliage. Viroid infections only rarely kill the host (Figs 3 and 4).
Viroid infections are also accompanied by a number of cytopathic effects - various chloroplast and cell wall abnormalities, the formation of membranous structures (so-called 'plasmalemmasomes' or
'paramural bodies') in the cytoplasm, and the accumulation of electron-dense deposits in both chloroplasts and cytoplasm. A combination of subcellular fractionation and in situ hybridization studies has shown that the plus and minus strands of PSTVd and related viroids both accumulate in the nucleolus. Precise partitioning between the nucleoplasm and nucleolus remains to be established, but this nucleolar localization may have important implications for replication and pathogenicity. ASBVd, in contrast, appears to be associated with chloroplast thalykoid membranes rather than the nucleoli of infected cells, thereby raisng the possibility that a host-encoded enzyme other than RNA polymerase II may be responsible for its replication (see below).
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