Cultured pulmonary intravascular macrophages (PIMS) and pulmonary alveolar macrophages(PAMS) were exposed to porcine reproductive and respiratory syndrome virus (PRRSV) (VR-2385) and infection was confirmed by an indirect immunofluorescence test and transmission electron microscopy. PRRSV did not affect the ability of PIMs or PAMs to internalize or kill Staphylococcus aureus, but significantly decreased the production of superoxide anion (SOA) and myeloperoxidase-H202-halide at 24 hours post infection (HPI). PIMs were as permissive as PAMs to infection either with low (ISU-55) or high (VR-2385) virulence PRRSV strains yielding similar progeny titers in vitro. However, PRRSV-infected PIMs from 4-week-old pigs killed fewer bacteria and yielded a higher virus titer than those from 4-month-old pigs at 48 HPI.;There was no difference in bactericidal activity between ISU-55- and VR-2385-infected PIMS. Both ISU-55 and VR-2385 infection significantly decreased the production of SOA at 24 and 48 HPI. Pulmonary clearance of copper particles was conducted to measure the effect of PRRSV infection on PIM function in vivo. Pigs were infused intravenously with 3% copper phthalocyanine tetrasulfonic acid (0.2 ml/kg) in saline 30 minutes prior to necropsy after 3, 7, 10, 14, or 28 days post infection (DPI) with uninfected-media, a modified-live virus vaccine (RespPRRS[superscript registered trademark symbol]), or a high virulence strain (VR-2385). Copper concentrations in the lungs of VR-2385-inoculated pigs were significantly lower than levels in the lungs of control and RespPRRS[superscript registered trademark symbol]-inoculated pigs at 7, 10, and 14 DPI.;The results suggest: 1) PIMs should be considered as an important replication site of PRRSV; 2) PRRSV had a detrimental effect on bactericidal acitivity and SOA production of PIMs in vitro; 3) PIMs from younger pigs were more permissive to PRRSV infection; 4) the selected PRRSV strains which differ in their abilities to induce pneumonia in vivo had no significant difference in vitro on virus titer and bactericidal functions; 5) the severity of PRRSV-induced damage to PIMs in vivo differs among PRRSV isolates; and 6) decreased pulmonary clearance of copper particles due to PRRSV infection supports the hypothesis that PRRSV infection may make pigs more susceptible to bacteremic diseases.