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The ultrastructural aspects of rotavirus SAll infection were studied in MA 104 cells, with particular attention directed to the early stages of virus adsorption and penetration. Within the first few minutes postadsorption, rotavirus was seen at the plasma membrane, associated with coated pits and coated vesicles, indicating that SAll virus is taken into the cell by adsorptive or receptor-mediated endocytosis. Multiple virus particles were seen, beginning at 1 h and continuing throughout infection, in lysosome-like structures. Ultrastructural evidence was obtained to support the hypothesis that rotavirus progeny acquire a temporary envelope by budding into cisternae of the rough endoplasmic reticulum.

The fastidious enteric adenovirus (FEAd) types 40 (Ad4O) and 41 (Ad4l) are found in stool specimens of infants and young children in association with gastroenteritis. Although they can be isolated routinely from clinical specimens by using 293 cells, they are propagated with variable success in cell lines which support the replication of other adenovirus serotypes. HeLa cells are generally considered to be nonpermissive for the replication of FEAds, but in this study, Ad4O and Ad4l grew to comparable titers in individual 293 and HeLa cells. However, virus was not efficiently released from infected HeLa cells and thus did not undergo multiple cycles of infection in HeLa cell cultures. The block in virus release was not overcome in KB18 cells which, like 293 cells, constitutively express proteins encoded by the E1B region of a subgroup C adenovirus (in this case Ad2). Moreover, it was apparent from these studies that Ad4O and Ad41 have particle-to-infectious unit ratios several orders of magnitude greater than that for AdS, even in 293 cells which express the ElA and E1B proteins of Ad5 and are considered to be permissive for replication of the FEAds. Neither the block in release of progeny virus nor the high particle-to-infectious unit ratio is explained solely by the defect in expression of the E1B 55K protein identified by Mautner et al. (V.

Aedes aegypti were infected with chikungunya virus by being fed on a blood–virus suspension poured over a sugar cube. The virus infection in the salivary glands was then studied with the electron microscope. In the proximal portion of the lateral lobes, 250–310 Å virus precursor particles were seen in the nucleus, in the cytoplasm, and on the membranes of cytoplasmic vesicles. Enveloped 500–580 Å virus particles with a 250–310 Å core were seen within the vesicles, in intercellular spaces, and in large numbers in the apical cavity and periductal space. In the distal portions of the lateral and median lobes precursor particles were present in the nucleus and cytoplasm, but no cytoplasmic vesicles were seen. Numerous enveloped virus particles were seen in the apical cavity and periductal space, and in the median lobe within the duct lumen as well. No evidence of virus replication was seen in the intermediate portion of the median lobe.In the distal portions, virus particles were frequently associated with a concentration of the secretory material. No other microscopically visible pathological changes were seen in the infected salivary glands.

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