Expression of the mouse hepatitis virus receptor by central nervous system microglia.
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.
Ramakrishna
Chandran
C
Department of Neurology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Bergmann
Cornelia C
CC
Holmes
Kathryn V
KV
Stohlman
Stephen A
SA
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002272:Carcinoembryonic Antigen / Q000378:metabolism*; D018352:Coronavirus Infections / Q000276:immunology / Q000821:virology; D015536:Down-Regulation; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D016513:Mice, SCID; D017628:Microglia / Q000166:cytology / Q000378:metabolism* / Q000821:virology; D006517:Murine hepatitis virus / Q000378:metabolism / Q000472:pathogenicity*; D011991:Receptors, Virus / Q000378:metabolism*
D002272:Carcinoembryonic Antigen; C486183:Ceacam1 protein, mouse; D011991:Receptors, Virus