Enteroviruses antagonize the host restriction factor ABL2 via proteasomal degradation to facilitate viral replication

Mengran Yuan1, Xiaorong Qiao1, Hua Wang1

  • 1Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, Department of Laboratory Medicine, School of Clinical Medicine & Laboratory Medicine, Jiangsu University, Zhenjiang 212013, China.

Virologica Sinica
|August 11, 2026
PubMed

Insights

Enteroviruses degrade the host protein ABL2 (Abelson murine leukemia 1-2) to promote infection. ABL2 acts as a restriction factor, inhibiting viral replication by downregulating RAC1 and the PI3K/AKT pathway.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Enteroviruses, such as Coxsackievirus B3 (CVB3), are major human pathogens causing severe diseases.
  • The role of ABL proto-oncogene 2 (ABL2) in enterovirus infection was previously unknown.

Purpose of the Study:

  • To investigate the interaction between enteroviruses and ABL2.
  • To elucidate the function of ABL2 in enterovirus infection and its underlying mechanism.

Main Methods:

  • Co-immunoprecipitation assays to detect protein interactions.
  • Western blotting to assess protein degradation and levels.
  • Analysis of viral replication in the presence and absence of ABL2.

Main Results:

  • Enteroviruses degrade host ABL2 via the ubiquitin-proteasome pathway mediated by viral protein 2B.
  • ABL2 functions as an antiviral restriction factor, inhibiting early viral replication.
  • ABL2 interacts with RAC1, downregulating its levels and suppressing the PI3K/AKT signaling pathway.

Conclusions:

  • Enteroviruses employ a post-translational mechanism to degrade ABL2, thereby evading host antiviral defenses.
  • ABL2's interaction with RAC1 and subsequent pathway modulation highlights a novel host-virus interplay.
  • Understanding this interaction provides a basis for developing new therapeutics against enteroviral diseases.

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