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ABSTRACT Detection of the mouse hepatitis virus receptor within the central nervous system (CNS) has been elusive. Receptor expression on microglia was reduced during acute infection and restored following immune-mediated virus control. Receptor down regulation was independent of neutrophils, NK cells, gamma interferon, or perforin. Infection of mice devoid of distinct inflammatory cells revealed CD4 + T cells as the major cell type influencing receptor expression by microglia. In addition to demonstrating receptor expression on CNS resident cells, these data suggest that transient receptor down regulation on microglia aids in establishing persistence in the CNS by assisting virus infection of other glial cell types.
CD4-Positive T-Lymphocytes, Mice, Inbred BALB C, Murine hepatitis virus, Down-Regulation, Mice, SCID, Carcinoembryonic Antigen, Mice, Inbred C57BL, Mice, Animals, Receptors, Virus, Microglia, Coronavirus Infections
CD4-Positive T-Lymphocytes, Mice, Inbred BALB C, Murine hepatitis virus, Down-Regulation, Mice, SCID, Carcinoembryonic Antigen, Mice, Inbred C57BL, Mice, Animals, Receptors, Virus, Microglia, Coronavirus Infections
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 24 | |
popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Average | |
influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |