@article{mbs:/content/journal/jgv/10.1099/0022-1317-75-8-1909, author = "Cassé, Huguette and Girerd, Yves and Gazzolo, Louis and Dodon, Madeleine Duc", title = "Critical involvement of human T cell leukaemia virus type I virions in mediating the viral mitogenic effect", journal= "Journal of General Virology", year = "1994", volume = "75", number = "8", pages = "1909-1916", doi = "https://doi.org/10.1099/0022-1317-75-8-1909", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-75-8-1909", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "Human T cell leukaemia virus type I (HTLV-I) is a direct activator of human resting T lymphocytes. The present study was undertaken to delineate further the role of viral particles and to define the involvement of envelope glycoproteins in the induction of T cell mitogenic stimulation. Virus-producing cells treated with paraformaldehyde (PFA) were found to be unable to induce the formation of syncytia, but still able to trigger the proliferation of resting T cells. Likewise, PFA-treated virus particles were still mitogenic. These results suggest that the mitogenic event is triggered before the fusion of the envelope with the cell membrane. Furthermore, HTLV-I envelope-expressing cells obtained after infection of C8166/45 cells (HTLV-I- transformed, but defective in virion production) with an HTLV-I envelope recombinant vaccinia virus were unable to activate normal T cells. Human immunodeficiency virus type 1 particles produced by C8166/45 cells were also devoid of mitogenic ability. However, when HTLV-I viral preparations were purified by chromatography, only the virion-containing fractions were found to be mitogenic for human resting T lymphocytes. This mitogenic activity was partially abolished by preincubating the purified virus with a monoclonal antibody directed to the surface envelope glycoprotein. Finally, treatment of HTLV-I-transformed cells by tunicamycin, an inhibitor of N-linked glyco-sylation, led to the production of virus particles with a decreased mitogenic activity. Collectively, these observations suggest that the HTLV-I mitogenic activity is triggered by the contact of HTLV-I virions with T cells.", }