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Original Article |
Among cells of the immune system, CD11c+ and DEC-205+ splenic dendritic cells primarily express the cellular receptor (
-dystroglycan [
-DG]) for lymphocytic choriomeningitis virus (LCMV). By selection, strains and variants of LCMV that bind
-DG with high affinity are associated with virus replication in the white pulp, show preferential replication in a majority of CD11c+ and DEC-205+ cells, cause immunosuppression, and establish a persistent infection. In contrast, viral strains and variants that bind with low affinity to
-DG are associated with viral replication in the red pulp, display minimal replication in CD11c+ and DEC-205+ cells, and generate a robust anti-LCMV cytotoxic T lymphocyte response that clears the virus infection. Differences in binding affinities can be mapped to a single amino acid change in the viral glycoprotein 1 ligand that binds to
-DG. These findings indicate that receptor–virus interaction on dendritic cells in vivo can be an essential step in the initiation of virus-induced immunosuppression and viral persistence.
Key Words: lymphocytic choriomeningitis virus CD11c+/DEC-205+ cells tropism viral receptor selection
-DG,
-dystroglycan; ECM, extracellular matrix; GP, glycoprotein; IDC, interdigitating dendritic cell; IS, immunosuppression phenotype; ko, knockout; LCMV, lymphocytic choriomeningitis virus; NP, nucleoprotein; P, persistence phenotype; RT, reverse transcriptase; S, small; VOPBA, virus overlay protein binding assay. © 2000 The Rockefeller University Press
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