Simian immunodeficiency virus induces expression of class II major histocompatibility complex structures on infected target cells in vitro

Abstract

The human immunodeficiency virus (HIV) and the closely related simian immunodeficiency virus (SIV) induce profound immune dysfunction in primate species. The present studies show that cell populations infected in vitro with SIV exhibit increases in major histocompatibility complex (MHC) class II antigen expression. Cell lines chronically infected with both the monkey and human viruses express substantially more MHC class H but not more lineage-restricted or activation antigens on their membranes than do uninfected cell lines. Furthermore, 2'-deoxy-5-iodouridine increased MHC class II antigen expression on SIV-infected cell lines in parallel with increased expression of viral antigens. MHC class II induction does not appear to be mediated through the production of a soluble factor, such as gamma interferon, by SIV-infected cells. Interestingly, studies of the kinetics of antigen expression by cell lines after SIV infection indicate that the induction of MHC class II structures is a late event. Immunoelectron microscopy revealed that MHC class II antigen is expressed not only on the surfaces of the SIV-infected cells but also on the envelope of virus particles derived from those cells. MHC antigen expression on virus-infected cells and the expression of those determinants by the virus may play a role in the pathogenesis of acquired immunodeficiency syndrome and the autoimmune abnormalities observed in HIV-infected individuals. * Corresponding author. fected with this isolate or those of H9 cells chronically infected with this isolate were used as a virus source. MAbs. Monoclonal antibodies (MAbs) reactive with Ti (24T6G12), T3 (2Ad2A2), T4 (19Thy5D7), MHC-I (W6/32), MHC-II (I-2,949), the interleukin-2 (IL-2) receptor (1HT4), and the T-cell activation antigen Ta.1 (4EL) were kindly provided by S. Schlossman (Dana-Farber Cancer Institute, Boston, Mass.). The anti-T3 MAb SP34 was provided by C. Terhorst (Dana-Farber Cancer Institute). The anti-MHC-II MAb LB3.1 was provided by J. Strominger (Dana-Farber Cancer Institute). All the anti-MHC-II MAbs used recognized HLA-DR. Cellular radioimmunoassay. Between 2 x 105 and 5 < 105

FIV infection of IL-2-dependent and -independent feline lymphocyte lines: Host cells range distinctions and specific cytokine upregulation

“…The upregulation of MHC class II noted in these ex vivo studies has also been reported with in vivo infection by FIV (Ohno et al, 1992;Rideout et al, 1992;Hunt and McConnell, 1995). Similar observations have also been noted with infections by HIV-1 (Cantin et al, 1997a, b) and SIV (Kannagi et al, 1987). At first glance, this would seem to be a counterproductive move for the virus in that it would, via class II-bound virus peptide, signal the immune system that the cell was infected and target it for clearing.…”

Ovine lentivirus is macrophagetropic and does not replicate productively in T lymphocytes

“…Infection and cellular activation. Lentivirus infection leads to increased expression of MHC class II antigens, an activation marker, on macrophages in infected sheep (32) and also in macaque cells (14,31) following infection. This prompted our investigation of the effect of virus inoculation on expression of activation antigens on PBMC.…”

CMV-induced class II antigen expression in various rat organs

“…In our previous studies [26,271, y-interferon-independent CMV-induced class I1 expression was recorded in rat heart endothelial cells in culture. Also, direct virus-induced class I1 expression has been demonstrated in other types of cells [12,17,181, indicating that viral agents, during binding, penetration, or replication, can cause some y-interferon-independent events that lead to class I1 expression in the target cells.…”

“…Class I1 expression, CMV. rat rect viral induction of class I1 molecules has been described for different cell types [12,17,18]. WF have previously demonstrated CMV-induced class I1 expression in rat heart endothelial cells in thdabsence of interferony [26,27], which suggests that a direct mechanism of upregulation of class I1 expression by the CMV might exist, at least in vitro.…”