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Related Experiment Video

Updated: May 20, 2025

Measuring Attachment and Internalization of Influenza A Virus in A549 Cells by Flow Cytometry
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Cellular SLC35B4 promotes internalization during influenza A virus entry.

Guangwen Wang1, Li Jiang1, Ya Yan1

  • 1State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, Heilongjiang, China.

Mbio
|March 25, 2025
PubMed
Summary

SLC35B4 is crucial for influenza A virus (IAV) replication by transporting UDP-xylose, aiding viral entry. This discovery highlights a new pathway for developing anti-IAV therapeutics.

Keywords:
AGRNAP2B1SLC35B4heparan sulfate modificationinfluenza A virusinternalization

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Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Influenza A virus (IAV) entry is a critical target for antiviral drug development.
  • Host factors mediating IAV replication are essential for understanding viral pathogenesis.

Purpose of the Study:

  • To identify host factors required for IAV replication using a genome-wide siRNA screen.
  • To elucidate the mechanism by which SLC35B4 facilitates IAV internalization and replication.

Main Methods:

  • Genome-wide siRNA screening to identify host factors for IAV replication.
  • Analysis of IAV replication stages in SLC35B4-deficient cells and knockdown mice.
  • Investigation of the heparan sulfate (HS) biosynthesis pathway and its role in IAV entry.
  • Assessment of protein homeostasis and interactions within the identified pathway.

Main Results:

  • SLC35B4 (nucleotide sugar transporter) is essential for IAV replication, independent of virus strain.
  • SLC35B4 facilitates IAV internalization by transporting UDP-xylose, crucial for heparan sulfate (HS) biosynthesis.
  • The HS biosynthesis pathway (XYLT2, B4GALT7, EXT1, EXT2) and AGRN are vital for IAV replication.
  • SLC35B4 regulates AGRN protein homeostasis via HS modification, impacting AP2B1 expression and IAV internalization.

Conclusions:

  • SLC35B4 is a key host factor promoting IAV replication and virulence through UDP-xylose transport.
  • The SLC35B4-mediated pathway involving HS biosynthesis and AGRN is critical for IAV internalization.
  • This axis presents a potential target for novel anti-IAV therapeutic strategies.