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Updated: Jun 16, 2026
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Author Spotlight: Elucidating the Pathways of TFH Cell Differentiation in Acute LCMV Challenges
Published on: April 26, 2024
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CD164 is a host factor for lymphocytic choriomeningitis virus entry
Mark J G Bakkers1, Alex Moon-Walker1,2,3,4, Rasmus Herlo5
1Department of Microbiology, Harvard Medical School, Boston, MA 02115.
Summary
Lymphocytic choriomeningitis virus (LCMV) uses host cell factors, including CD164 and alpha-dystroglycan (α-DG), for entry. The virus switches receptors during entry, offering new therapeutic targets.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Lymphocytic choriomeningitis virus (LCMV) is a zoonotic arenavirus transmitted by rodents.
- LCMV infection can lead to severe congenital abnormalities and is a significant risk for transplant recipients.
Purpose of the Study:
- To identify host factors essential for LCMV entry into host cells.
- To elucidate the mechanism of LCMV cell entry and identify potential therapeutic targets.
Main Methods:
- Genome-wide loss-of-function screen to identify host factors.
- Biochemical analysis of LCMV glycoprotein interactions.
- Cellular entry pathway analysis.
Main Results:
- Identified CD164, glycosylation factors, heparan sulfate machinery, and alpha-dystroglycan (α-DG) as host factors for LCMV entry.
- LCMV glycoprotein binds CD164 at acidic pH, requiring a sialylated glycan.
- LCMV entry involves a switch from initial binding (heparan sulfate or α-DG) to CD164 before membrane fusion.
Conclusions:
- CD164 is a novel, critical host factor for LCMV cell entry.
- The identified host factors and entry mechanism provide new targets for antiviral therapies against LCMV.
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