Viral induction, transmission and apoptosis among cells infected by a Human Intracisternal A-type retrovirus
Sjogren’s Syndrome, a systemic autoimmune disease, is characterized by lymphocytic infiltration of the salivary or lacrimal glands, producing xerostomia or xerophthalmia. Although definitive proof of viral etiology has not been established, a cell line containing viral particles termed Human Intraci...
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Published in: | Virus research Vol. 61; no. 1; pp. 19 - 27 |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Netherlands
Elsevier B.V
01-05-1999
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Subjects: | |
Online Access: | Get full text |
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Summary: | Sjogren’s Syndrome, a systemic autoimmune disease, is characterized by lymphocytic infiltration of the salivary or lacrimal glands, producing xerostomia or xerophthalmia. Although definitive proof of viral etiology has not been established, a cell line containing viral particles termed Human Intracisternal A-type Particles (HIAP) resulted from co-culture with patient lip biopsies. We stimulated these chronically infected cells with phorbol myristate acetate (PMA) in an effort to enhance production of viral particles for further characterization. We report that the virus present in the HIAP cell line can be induced to become lytic when subjected to PMA and that there is a difference in the effects of PMA on H9 and HIAP cell groups, with apparent protection from apoptosis due to PMA being exerted by viral presence. Delayed apoptosis may prolong exposure of the foreign/self complex, thus enhancing an autoimmune response. Polyacrylamide gel electrophoresis (PAGE) revealed the presence of new peptides in pellets of supernatants of PMA-stimulated HIAP cells, with prominent bands at 55 and 43 kDa, and several fainter ones. HIAP infection was transferred by cell-free filtered supernatants from stimulated cells to H9 cells, which became identical to parent HIAP cells by PAGE and fluorescence activated cell sorter. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 0168-1702 1872-7492 |
DOI: | 10.1016/S0168-1702(99)00021-0 |