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Observational analysis reveals unconventional nucleus export and secondary necrosis in Jurkat cells, suggesting structural changes due to HIV-1 transcription.
Efficient transcriptional activation and replication of the human immunodeficiency virus (HIV-1) is dependent on Tat protein. Initial observations have shown that human leukemia T lymphocytes (Jurkat cells aka Wild type or WT) transfected with HIV-1 LTR CAT TAT-72 plasmid as Control (CTJ) cells, and CTJ transfected by electroporation with pcDNA3-pU3R-CAT-TAT-72 (TJ cells) showed growth and maintenance resulting in giant and small cells with accumulated corpses. The lack of fine structure in Jurkat cells and both transfected cells aimed at us to verify their respective ultrastructure modifications. Scanning and transmission electron microscopy showed evident Cajal bodies in CTJ cells compared with WT cells and revealed unconventional nucleus export of viral-associated transcripts where eruption of the nucleus envelope spilled content from the perinuclear space toward exocytosis via a lined membranous channel continuum of endoplasmic reticulum – mitochondria envelope. TJ cells grew as small and giant cells where giant cells bore virological synapses stimulating apoptogenic impetus but where cell demise included osmotic bursts mostly resulted into secondary necrosis. Jurkat transfected cells could model in vitro resilient human T lymphocytes (or other infected cells) that remain factories of expressed HIV-1 virus proteins such as Tat, secreted and captured by other cells as in viral infections and can form giant cells. Those Tat and other transcripts induced cell demise, as in vivo those HIV-1 viral proteins and traces can amplify infectivity as in AIDS, altering primary lymphoid organs and secondary lymphoid organs.
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Gilloteaux et al. (2025) studied this question.
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