Abstract
Although phagocytic cells of the RES have been identified as a critical determinant of host resistance in certain viral diseases, the mechanism remains only partially defined. We utilized an in vitro experimental model system to better define the capacity of macrophages to control a virus infection in the absence of other components of the host's defense mechanism. Progression of a vaccinia virus infection in cultures of mouse embryo fibroblasts was partially controlled, as evidenced by decreased (1) foci of cell destruction (CPE) and (2) extracellular virus, in cultures receiving mouse peritoneal macrophages and lymphocytes. This protective effect was shown to be predominantly mediated by the macrophages after separation on a Ficoll density gradient. Nonspeclfically activated macrophages (from BCG immunized mice) had a significantly enhanced capacity to control virus replication. Interferon could not be detected and the suppression of virus replication occurred in the absence of significant virus uptake by the macrophages. These data support the concept that (1) RES cells contribute to host resistance in certain virus infections and (2) suggest that macrophages may directly interact with virus-infected cells and block production or release of progeny virus.
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Glasgow, L., Murrer, A. ROLE OF RETICULOENDOTHELIAL SYSTEM (RES) MACROPHAGES IN HOST RESISTANCE TO VIRAL INFECTIONS. Pediatr Res 8, 425 (1974). https://doi.org/10.1203/00006450-197404000-00508
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DOI: https://doi.org/10.1203/00006450-197404000-00508