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CD164 is a host factor for lymphocytic choriomeningitis virus entry
Author(s) -
Mark J. G. Bakkers,
Alex Moon-Walker,
Rasmus Herlo,
Vesna Brusic,
Sarah H. Stubbs,
Kathryn M. Hastie,
Erica Ollmann Saphire,
Tomas Kirchhausen,
Sean P. J. Whelan
Publication year - 2022
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2119676119
Subject(s) - lymphocytic choriomeningitis , heparan sulfate , biology , virus , glycosylation , glycoprotein , virology , arenavirus , glycan , microbiology and biotechnology , biochemistry , cell , cytotoxic t cell , in vitro
Significance Lymphocytic choriomeningitis virus (LCMV) is the prototypic arenavirus and has been utilized for decades as a model to understand the host immune response against viral infection. LCMV infection can lead to fatal meningitis in immunocompromised people and can lead to congenital birth defects and spontaneous abortion if acquired during pregnancy. Using a genetic screen, we uncover host factors involved in LCMV entry that were previously unknown and are candidate therapeutic targets to combat LCMV infection. This study expands our understanding of the entry pathway of LCMV, revealing that its glycoprotein switches from utilizing the known receptor α-DG and heparan sulfate at the plasma membrane to binding the lysosomal mucin CD164 at pH levels found in endolysosomal compartments, facilitating membrane fusion.

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