Respiratory syncytial virus G‐protein modulates cytokine release from human peripheral blood mononuclear cells

Respiratory syncytial virus (RSV) is the major cause of lower respiratory tract infection in children and adults. In vivo the host has to cope with intact replicative virus, with non-replicative virus, and/or with viral structural proteins including the outer membrane G-protein. We analyzed the role of purified RSV G-protein with regard to its modulatory efficacy for interleukin (IL) -10, IL-12, and tumor necrosis factor-a (TNF-cz) release from human pe- ripheral blood mononuclear cells (PBMC). These cytokines seem to contribute to the deleterious effect in viral infections. Treatment of PBMC with RSV at a multiplicity of infection of 10 down to 0.00 1 induced the release ofTNF-a, IL-b, and IL-12; also time kinetics and dose-responses differed markedly. Stimulation of PBMC with purified RSV G-protein (from 0.001 up to 10 �.tg/106 PBMC) led only to a pronounced increase in IL-lO within a concentration range from 0.01 up to 0.5 �.tg/106 PBMC with a maximum between 12 and 18 h of incubation. At later time points (24, 48, and 72 h) G-protein concentrations above 1 �.tgJ106 PBMC suppressed IL-b, TNF-a, and IL-12 release from human PBMC. Coating of PBMC with RSV G-protein sup- pressed IL-lO, TNF-a, and IL-12 release after sub- sequent stimulation with RSV. Our data indicate a regulatory role of RSV G-protein for immune re- sponses toward viral infection. J. Leukoc. Biol. 59: 403-406; 1996.