Non-crystalline inclusions, referred to as X-bodies, developed in leaf-hair cells of infected with a RNA-producing defective isolate () of tobacco rattle virus but not in those infected with the nucleoprotein particle-producing strain () from which was derived. The X-bodies appeared 3 days after inoculation; some persisted for at least 10 weeks. They were digested by pronase and were rich in RNA, which was protected by proteinaceous material from digestion by pancreatic ribonuclease; they did not contain virus coat-protein detectable by fluorescent antibody tests. Electron microscopy of thin sections showed that mitochondria in infected cells developed two abnormalities—peripheral membranous sacs and membrane bounded vacuoles—and then aggregated, together with ribosomes and material containing small darkly staining granules, to form small X-bodies. These fused to form larger X-bodies, in which the mitochondria were further modified and eventually became barely recognizable. Finally, the contents of the X-bodies became increasingly amorphous, and the bodies disintegrated.

X-bodies also developed in leaf-hair cells infected with the virus particle-producing strain , but were less common and mostly persisted for only a few days. These X-bodies were formed in the same way as those produced by , but contained in addition small aggregates of virus particles resembling the aggregates found in the cytoplasm in other parts of the same cells. The frequency of formation, and persistence, of X-bodies induced by these tobacco rattle viruses paralleled the severity and persistence of their macroscopic effects on . The possibility that mitochondria are sites of synthesis of tobacco rattle virus RNA is discussed.


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