%0 Journal Article %A Schnorr, Jens-Jörg %A Seufert, Marion %A Schlender, Jörg %A Borst, Jannie %A Johnston, Ian C. D. %A Meulen, Volker ter %A Schneider-Schaulies, Sibylle %T Cell cycle arrest rather than apoptosis is associated with measles virus contact-mediated immunosuppression in vitro %D 1997 %J Journal of General Virology, %V 78 %N 12 %P 3217-3226 %@ 1465-2099 %R https://doi.org/10.1099/0022-1317-78-12-3217 %I Microbiology Society, %X Acute measles is associated with pronounced immunosuppression characterized both by leukopenia and impaired lymphocyte functions. In an earlier study, we found that mitogen-dependent proliferation of uninfected human peripheral blood lymphocytes (PBLs) and spontaneous proliferation of human cell lines of lymphocytic or monocytic origin was impaired after contact with UV- inactivated, measles virus (MV)-infected cells, UV- inactivated MV or with cells transfected with MV glycoproteins (gp) F and H. We now show that mitogen-stimulated PBLs and Jurkat cell clones either highly sensitive or resistant to CD95-induced apoptosis have a similar sensitivity to MV-induced inhibition and do not undergo apoptosis. Moreover, unimpaired mitogen-dependent upregulation of important activation markers, including IL-2R, was observed in PBL cultures after contact with MV- infected, UV-irradiated presenter cells. This indicates that the cells were indeed viable and acquire a state of activation. Less IL-2 was released from PBLs after contact with MV-infected presenter cells when compared with that released after contact with uninfected cells. However, mitogen-induced proliferation of PBLs was not restored by addition of IL- 2 under these conditions. It appeared that a higher fraction of mitogen-stimulated PBLs accumulated in the G0/G1 phase of the cell cycle after contact with MV-infected cells. Thus, the mitogen- unresponsiveness of PBLs seen after contact with MV-infected cells is due to cell cycle arrest rather than apoptosis. %U https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-78-12-3217