Suppressed expression of ICAM-1 and LFA-1 and abrogation of leukocyte collaboration after exposure of human mononuclear leukocytes to respiratory syncytial virus in vitro. Comparison with exposure to influenza virus

Abstract

Human mononuclear leukocytes (MNL) exposed to respiratory syncytial virus (RSV) produce net IL-1 inhibitor bioactivity with the anticipated consequences of cell cycle arrest, suppressed virus-specific proliferation, and reduced expression of activation markers. These studies were undertaken to investigate effects of exposure and resultant net IL-1 inhibitor activity on the expression of the intercellular adhesion molecule-1 (ICAM-1), and its ligand the lymphocyte function-associated antigen (LFA-1). MNL collected at 1, 4, and 24 h after exposure to influenza virus (which induces net IL-1 bioactivity) showed enhanced expression of ICAM-1 and LFA-1 relative to sham-exposed MNL and exhibited cell clustering. In contrast, exposure to RSV was associated with suppressed expression of both ICAM-1 and LFA-1 and with minimal detectable cell clustering throughout the culture period. Influenza virus-exposed MNL produced significantly more IL-1 and IFN-gamma (which require cell-cell collaboration for optimal production) than did RSV-exposed MNL. These data raise the possibility that exposure of MNL to RSV fails to elicit or blocks the early events necessary for cellular collaboration, contributing to early suppression of the clonal expansion of RSV-specific lymphocytes.