Infection of Cultured Murine Brain Cells by Semliki Forest Virus: Effects of Interferon-αβ on Viral Replication, Viral Antigen Display, Major Histocompatibility Complex Antigen Display and Lysis by Cytotoxic T Lymphocytes Morris, A. and Tomkins, P. T. and Maudsley, D. J. and Blackman, M.,, 68, 99-106 (1987), doi = https://doi.org/10.1099/0022-1317-68-1-99, publicationName = Microbiology Society, issn = 0022-1317, abstract= SUMMARY Primary brain cell cultures prepared from newborn mice were infected with Semliki Forest virus (SFV). The effects of interferon (IFN-α β) treatment on SFV replication, SFV and major histocompatibility complex (MHC) class I antigen expression, and susceptibility to lysis by SFV-specific cytotoxic T lymphocytes (CTL) were determined. The IFN-αβ treatment prevented replication of SFV as determined by incorporation of [3H]uridine into SFV RN A and very markedly reduced the expression of SFV antigens on the cell surface as determined by lysis with antibody and complement or indirect immunofluorescence. However, IFN-aJ? increased expression of MHC class I antigens, measured by indirect immunofluorescence and as assessed indirectly by susceptibility to killing by alloreactive T cell lines. SFV infection had no effect on MHC class I expression in either IFN-αβ -treated or -untreated cells. The infected IFN-αβ-untreated brain cells were susceptible to killing by the CTL at effector/target ratios in the range 3 to 30. The killing was MHC antigen-restricted, and uninfected cells were not killed. A target cell (YAC) highly susceptible to natural killer cell cytotoxicity was not killed by the CTL. IFN-αβ treatment prior to SFV infection resulted in an augmentation of lysis by the CTL, indicating that even where SFV antigen expression is reduced, in the context of enhanced MHC class I expression brain cells remain susceptible to CTL killing., language=, type=