Advances in Insect Physiology, Vol. 25 by P. D. Evans

By P. D. Evans

Insect body structure is at the moment present process a revolution with the elevated software of molecular organic concepts to enquire the molecular mechanisms underlying the physiological responses to insect cells. Advances in Insect body structure has instituted a dedication to the booklet of top quality experiences on molecular biology and molecular genetics in parts the place they supply an elevated knowing of physiological approaches in bugs. quantity 25 includes elevated assurance at the molecular biology of insect body structure.

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The first recognizable viral structures are incomplete crescent-like shells or membranes appearing at the periphery of the virogenic stroma. These membranes develop and eventually enclose a mass of electron-dense material. Electron micrographs have shown that these immature particles consist of an inner trilaminar structure of unit membrane and a spicule coat (Stoltz and Summers, 1972). In type I1 viroplasms, crescent or arch-like envelopes are present in association with fibrillar material containing a large number of vesicles (Bergoin et a f .

Acrea larvae infected with Amsacta moorei (Am) EPV is frequently preceded by paralysis of the abdomen and by regurgitation or defecation of fluid containing virus. The primary site of virus multiplication is in the cytoplasm of fat body cells, although mid-intestinal cells, hypodermis, muscle cells, tracheoblasts, haemocytes and ganglion connective tissue are also affected (Roberts and Granados, 1968). The infection of Lepidopteran pupae by some EPVs has been reported (Retnakaran and Bird, 1972; Sutter, 1972), however, infections of the adult stage are not known.

Most studies have been carried out with AmEPV infections of E. acrea larvae. Infection begins when larvae ingest viral occlusion bodies which dissolve in the alkaline environment of the gut to release virus particles. Granados (1973b) observed that AmEPV was first detected in the gut lumen 1-2 h after per 0s inoculation of E. acrea larvae. The viral envelope then fuses with the plasma membrane of microvilli and subsequently the viral core and lateral bodies enter the cell cytoplasm. , 1971). Following uncoating and a period of latency, cytoplasmic foci consisting of either electron-dense amorphous material (type I viroplasm), or aggregates of granular material interspersed with spherical vesicles (type I1 viroplasm) begin to appear in infected cells.

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