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A Calcium Bioluminescence Assay for Functional Analysis of Mosquito Aedes aegypti and Tick Rhipicephalus microplus G Protein-coupled Receptors
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LRP8 is a receptor for tick-borne encephalitis virus

Eva Mittler1, Alexandra L Tse2, Pham-Tue-Hung Tran3

  • 1Department of Microbiology and Immunology, Albert Einstein College of Medicine, New York, NY, USA. eva-maria.mittler@einsteinmed.edu.

Nature
|September 24, 2025
PubMed

Insights

Researchers identified LRP8 as a key receptor for tick-borne encephalitis virus (TBEV) entry into cells. Blocking LRP8 protected human cells and mice from TBEV infection, offering new therapeutic strategies.

Area of Science:

  • Virology
  • Neuroscience
  • Immunology

Background:

  • Tick-borne encephalitis virus (TBEV) causes severe neuroinflammation and is a significant public health concern.
  • Host factors mediating TBEV entry into the central nervous system are not well understood.
  • Orthoflaviviruses, like TBEV, are enveloped RNA viruses transmitted by arthropods.

Purpose of the Study:

  • To identify host factors essential for TBEV entry and infection.
  • To investigate the role of identified factors in viral neuropathogenesis.
  • To explore potential therapeutic targets for TBEV infection.

Main Methods:

  • Genome-scale CRISPR-Cas9 screening was employed to identify host cell receptors for TBEV.
  • LRP8 function in TBEV infection was assessed through downregulation and overexpression studies in human cells.
  • Direct binding assays between LRP8 and the TBEV E glycoprotein were performed.
  • Viral attachment and internalization mediated by LRP8 were analyzed.
  • An LRP8-based soluble decoy was developed and tested for antiviral efficacy in cell lines, neuronal cells, and a mouse model.

Main Results:

  • LRP8, a receptor for apolipoprotein E and reelin, was identified as a critical TBEV receptor.
  • Downregulation of LRP8 significantly reduced TBEV infection, while its overexpression enhanced it.
  • LRP8 directly binds to the TBEV E glycoprotein, facilitating viral attachment and cell entry.
  • An LRP8-based soluble decoy effectively blocked TBEV infection in various cell types and protected mice from lethal challenge.

Conclusions:

  • LRP8 is a crucial host factor for TBEV entry, mediating viral attachment and internalization.
  • Targeting LRP8 presents a promising strategy for developing novel antiviral therapies against TBEV.
  • Understanding LRP8's role advances knowledge of TBEV neuropathogenesis and potential treatment avenues.

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