acid-phosphatase and Cytomegalovirus-Infections

We have shown that normal C57BL/6J mice are moderately resistant to infection with murine cytomegalovirus (MCMV) and that this resistance is impaired by prior infection with LP-BM5 MuLV, which causes a disease (MAIDS) similar to early HIV-induced disease. This study investigates macrophage function in MAIDS+ mice challenged with MCMV. MAIDS reduces the influx of cells into the peritoneal cavity seen in normal C57BL/6J mice 6 days after MCMV infection. The infiltrates contained cells that resembled activated macrophages, as they took up colloidal gold, expressed the macrophage marker Mac-1, had high levels of acid phosphatase activity, and were lymphocytostatic when co-cultured with activated T cells. MAIDS+ mice had a higher percentage of cells able to take up colloidal gold and higher acid phosphatase activity per cell. The cells were also more lymphocytostatic and produced higher levels of interleukin-1 and tumor necrosis factor-alpha on days 4 and 6 after MCMV infection. Hence, MAIDS enhances baseline and induced macrophage activity, but depresses infiltration into the site of inflammation.

Topics: Acid Phosphatase; Animals; Cells, Cultured; Coculture Techniques; Cytomegalovirus; Cytomegalovirus Infections; Female; Flow Cytometry; Inflammation; Interleukin-1; Lymphocyte Activation; Macrophage Activation; Macrophage-1 Antigen; Macrophages, Peritoneal; Mice; Mice, Inbred C57BL; Murine Acquired Immunodeficiency Syndrome; T-Lymphocytes; Time Factors; Tumor Necrosis Factor-alpha

Structural and functional changes were studied in murine peritoneal macrophages infected with murine cytomegalovirus by using centrifugal enhancement to achieve a high-level (greater than 90%) pulsed infection. During 3 d of culture the infected cells became enlarged and rounded with smooth surface contours. Transmission electron microscopy demonstrated various stages of viral maturation in the nucleus and cytoplasm. Intracellular organization was generally retained, apart from the development of large, irregular, intracytoplasmic vacuoles, in which enveloped virions and cell debris accumulated. The infected macrophages lost most surface markers tested (F4/80, Mac-1, FcR, and the receptor for gluteraldehyde-fixed sheep red blood cells), but H-2 expression was increased. Moreover, ingestion of colloidal gold or horseradish peroxidase was depressed, and the levels of acid phosphatase activity, lymphocytostatic activity, and interleukin 1 production were also decreased. The latter may explain the observed loss of accessory cell function.

Topics: Acid Phosphatase; Animals; Antigen-Presenting Cells; Antigens, Differentiation, Myelomonocytic; Antigens, Viral; Cytomegalovirus; Cytomegalovirus Infections; Female; Interleukin-1; Macrophages; Mice; Mice, Inbred BALB C; Microscopy, Electron; Pinocytosis; RNA; Virus Replication

Topics: Acid Phosphatase; Adenovirus Infections, Human; Arachis; Carboxylic Ester Hydrolases; Chickenpox; Cytomegalovirus Infections; Humans; Influenza, Human; Measles; Paramyxoviridae Infections; Pneumonia, Viral; Receptors, Mitogen; Respiratory Syncytial Viruses; Respirovirus Infections

Topics: Acid Phosphatase; Alkaline Phosphatase; Analysis of Variance; Animals; Cytomegalovirus; Cytomegalovirus Infections; Cytopathogenic Effect, Viral; Female; Histocytochemistry; Hot Temperature; Liver; Mice; Mice, Inbred Strains; Regression Analysis; Time Factors; Tissue Extracts

Topics: Acid Phosphatase; Cytomegalovirus; Cytomegalovirus Infections; Electrons; Herpesviridae; Histocytochemistry; Lysosomes; Microscopy; Microscopy, Electron; Research; Tissue Culture Techniques; Virus Cultivation

Topics: Acid Phosphatase; Alkaline Phosphatase; Bile; Cell Nucleus; Cholestasis; Cytomegalovirus Infections; Giant Cells; Hepatitis; Humans; Infant; Infant, Newborn; Jaundice; Liver; Liver Diseases; Liver Regeneration; Pathology