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I Tariska

Publications and source records attributed to I Tariska.

8 recordsLinked to original sources
PubMed1982

Are astrocytes infected in progressive multifocal leukoencephalopathy (PML)?

Ultrastructural characteristics of the early steps of PML virus infection, i.e. adsorption, penetration, and intracellular virus transport were demonstrated in astrocytes. These phenomena were more frequently seen in the cytoplasm than virus assembly in the nuclei. Infection of the astrocytes is usually non-productive. Light- and electron-microscopic analysis of the present case and 23 cases published in the literature since 1970 leads to the conclusion that the relation is inverse between the appearance of giant, bizarre astrocytes and that of the productive infection of the non-transformed one. The transformation of the astrocytes seems to be induced by infection with the PML virus.

Astrocytes↗
PubMed1980

Morphological demonstration of the first phase of polyomavirus replication in oligodendroglia cells of human brain in progressive multifocal leukoencephalopathy (PML).

Ultrastructural characteristics of adsorption, penetration and intracellular transport of polyomavirus is demonstrated in oligodendrocytes in PML. The findings are compared with those obtained by virological examinations of polyomavirus infections described in cell cultures. The morphology of the eclipse phase and the site of the beginning of virus assembly are also described. The vacuolization of the cytoplasm is considered to be the consequence of the production of viral protein and nucleic acid. The cytoplasmic virions surrounded by membrane in the early and late phases of replication are considered to be "infective virions", while those in the cytoplasm in a "free" state, aligned along membrane fragments or arranged in crystals are classified as "virus progenies". The first demonstration of polyoma virions between the separated lamellae of the myelin sheath of a viable axon is presented; their presence, however, is not considered to play a direct pathogenetic role in demyelination.

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