Symptoms on systemically infected hosts range from undetectable to moderate, depending on the individual potexvirus. Generally, systemic symptoms include chlorotic mottle or mosaic patterns, with stunting also being common. Potexviruses are capable of infecting most host tissues. Both primary and systemic cytopathology can occur in a single host. Gomphrena globosa is the most common local lesion host among members of the potexvirus group.

Inclusion bodies, composed of potexvirus particles packed in parallel arrays, often form in the cytoplasm and sometimes in the nucleus of infected cells. These aggregates often vary in size and have irregular shapes, but can form spindle-shaped structures in some potexviruses. Another type of inclusion, laminated inclusion components (LIC), are thin protein-aceous sheets associated with bead-like structures. LICs display no viral antigens. A third type, the amorphous inclusions, occur in the cytoplasm and vacuoles. Amorphous inclusions contain viral antigens.

Co-infecting a single host with a potexvirus and another virus (e.g. a potyvirus) can have a synergistic effect on symptoms. For instance, mixed infections with PVX and potato virus Y (PVY) produces a dramatic increase in the severity of PVX symptoms, pathogenicity and accumulation, compared to that observed by infection with PVX alone. Other poty-viruses such as tobacco vein mottling virus (TVMV), tobacco etch virus (TEV) and pepper mottle virus are also capable of the synergistic effect on PVX replication and symptom severity. The replication of the entire potyviral genome is not increased nor required for PVX/potyviral synergism. The synergistic response is mediated by expression of the 5'-proximal third of the genomic potyviral RNA (i.e. protease-1, helper component protease (HC-Pro) and protein-3 gene). The exact molecular basis for PVX/PVY synergism is not presently well understood.

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