Respiratory syncytial virus infection of neonatal monocytes stimulates synthesis of interferon regulatory factor 1 and interleukin-1beta (IL-1beta)-converting enzyme and secretion of IL-1beta.

Interleukin-1beta (IL-1beta) production in response to respiratory syncytial virus (RSV) was investigated in normal neonate monocytes. Intracellular or culture supernatant IL-1beta protein levels were measured by enzyme immunoassay. The expression of mRNAs for interferon regulatory factor 1 (IRF-1), IL-1beta-converting enzyme (ICE), and IL-1beta in the cells was analyzed semiquantitatively by reverse transcriptase-PCR. Before RSV exposure, some IRF-1, ICE, and IL-1beta transcripts were already expressed in the monocytes. The levels of these transcripts increased significantly 2 h after RSV exposure compared with those in mock-infected cells. At that time, significantly higher intracellular IL-1beta protein levels were observed in RSV-exposed cells. After 20 h of RSV exposure, quantities of soluble IL-1beta secreted from RSV-exposed cells were moderately higher than those from noninfected cells. These observations suggest that RSV infection of neonatal monocytes triggers enhanced transcription and increased translation of the IL-1beta gene and increased secretion of the soluble protein. The later phase of these processes may be promoted by ICE activity, which was upregulated by increased IRF-1. The increase in IRF-1 activity may also result from RSV infection.