We proposed that clarithromycin efficiently suppressed PAF receptor-mediated Streptococcus pneumoniae adhesion to respiratory epithelial cells as well as RSV-induced proinflammatory cytokine and chemokine production. Clarithromycin may suppress secondary bacterial infections and immunological disorders during RSV infection. Post-Transcriptional Control of Type I Interferon Induction by Porcine Reproductive and Respiratory Syndrome Virus in Its Natural Host Cells Porcine reproductive and respiratory syndrome virus (PRRSV) is not only a poor inducer of type I interferon but also inhibits the efficient induction of type I interferon by porcine transmissible gastroenteritis virus (TGEV) and synthetic dsRNA molecules, Poly I:C. However, the mechanistic basis by which PRRSV interferes with the induction of type I interferon in its natural host cells remains less well defined. The purposes of this review are to summarize the key findings in supporting the post-transcriptional control of type I interferon in its natural host cells and to propose the possible role of translational control in the regulation of type I interferon induction by PRRSV. Porcine reproductive and respiratory syndrome virus (PRRSV) is a single-stranded, positive-sense RNA virus with a genome size of approximately 15 kb. PRRSV belongs to the Arteriviridae in the order of Nidovirale. PRRSV causes acute respiratory disease in neonatal and young piglets and reproductive failure in pregnant sows. PRRSV primarily infects and destroys alveolar macrophages during acute infection of swine. In addition to macrophages, PRRSV has also been identified by immunohistochemistry in dendritic-like cells in tonsils and lymph nodes [1] , suggesting that dendritic cells may either be susceptible to PRRSV or capture PRRSV by taking up apoptotic infected cells.