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LRP8 is a functional receptor for yellow fever virus
Miao Mei1, Yang Yang2, Zihan Zhang3,4
1Beijing Key Laboratory of Autoimmune Disease Mechanism Research and Novel Drug Development, Chinese Institute for Immunology, Chinese Institutes for Medical Research, Capital Medical University, Beijing, China.
Nature Microbiology
|March 20, 2026
Summary
Researchers identified LRP8 (apolipoprotein E receptor 2) as a key receptor for yellow fever virus (YFV) entry. This discovery enhances understanding of YFV infection and pathogenesis.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Yellow fever virus (YFV) is a significant arbovirus causing severe human illness and death.
- The widely used 17D vaccine strain highlights the importance of understanding YFV biology.
- The specific cellular receptors utilized by different YFV strains are not fully understood.
Purpose of the Study:
- To identify the cellular receptor(s) involved in yellow fever virus (YFV) entry.
- To elucidate the role of identified receptors in YFV infection and pathogenesis.
Main Methods:
- Conducted a genome-wide human open-reading frame library screen using barcoded technology.
- Utilized cell lines, primary human hepatocytes, mosquitoes, and a mouse model for infection studies.
- Performed biochemical assays to confirm direct interaction between YFV and the identified receptor.
Main Results:
- Identified LRP8 (apolipoprotein E receptor 2) as a functional receptor for YFV.
- Demonstrated that LRP8 expression enhances YFV infection by promoting viral entry in various cell types.
- Showed that LRP8 knockdown reduces YFV infection in multiple tissues and vectors.
- Confirmed direct interaction between LRP8 and YFV envelope protein, with soluble LRP8 blocking infection.
Conclusions:
- LRP8 is a critical receptor for yellow fever virus entry, influencing infection and tropism.
- Targeting the LRP8-YFV interaction may offer new strategies for YFV prevention and treatment.
- Findings provide fundamental insights into YFV pathogenesis and host-pathogen interactions.
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