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SV40-induced transformation of human diploid cells: Crisis and recovery

✍ Scribed by Girardi, A. J. ;Jensen, F. C. ;Koprowski, H.


Publisher
Wiley (John Wiley & Sons)
Year
1965
Tongue
English
Weight
1002 KB
Volume
65
Category
Article
ISSN
0095-9898

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✦ Synopsis


Nineteen cultures of human embryonic or adult-tissue cells were exposed to sv40 as primary cultures or developed cell strains in Phase I1 of cultural life; 12 cultures were exposed to virus in Phase 111, at the end of in vitl-o life. After the expected proliferative response, infected cultures exhibited morphological change, accelerated growth, and prolongation of propagability. After a n average of 22.6 weeks for cultures infected as primary explants or in Phase 11, the proliferative stage of transformation ended in a stage of "crisis." Crisis was characterized by progressive decline in vigor of culture proliferation, increasingly abnormal cell division, and limitation i n propagability of cells eventually resulting in diminution i n cell number. Cytological features of crisis included detachment of cells and appearance of multinucleated and giant cells. Temporally and cytologically, crisis was similar for transformed cells whether of adult or embryonic origin, whether derived from skin, buccal mucosa or lung, whether in Phase I1 or I11 of culture life at the time of infection (the "older" cultures entering crisis sooner than the "younger"), and whether propagated continuously or with intervening periods of growth arrest or proliferation in vivo. After a variable time "recovery" of cultures from crisis occurred by repopulation from small groups of surviving but seemingly dormant cells. The new populations, always obtained with care of cultures i n crisis, formed continuously propagable cell lines. Control uninfected cultures have always exhibited the finite life terminating in Phase I11 which is characteristic of human diploid cell strains. Passage of transformed cultures through crisis and recovery was accompanied by loss of capacity to release infectious SV40 and enhancement of production of SV40-induced complement-fixing antigen.


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