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Updated: May 20, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

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Published on: March 2, 2014

HCMV-pUS2 Disrupts cGAS-STING Signaling through LMAN2L Degradation.

Yue-Peng Zhou1,2,3, Yong-Xuan Yao4, Jin-Peng Wu1,2

  • 1State Key Laboratory of Virology and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.

Plos Pathogens
|May 18, 2026
PubMed
Summary

Human cytomegalovirus (HCMV) evades immune responses by degrading the host protein LMAN2L, a key STING pathway regulator. The viral protein pUS2 targets LMAN2L for degradation, hindering antiviral defenses.

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Human cytomegalovirus (HCMV) employs sophisticated immune evasion tactics.
  • The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is crucial for innate antiviral immunity.

Purpose of the Study:

  • To identify novel HCMV immune evasion mechanisms targeting the cGAS-STING pathway.
  • To elucidate the role of host factor LMAN2L in STING pathway regulation and HCMV infection.

Main Methods:

  • Investigated HCMV-induced degradation of LMAN2L using viral infection models.
  • Utilized molecular biology techniques to identify HCMV pUS2, E3 ligase RNF139, and E2 enzyme UBE2G2 in LMAN2L degradation.
  • Examined the impact of LMAN2L knockout on type I interferon responses and STING pathway activation.
  • Analyzed LMAN2L interaction and co-localization with STING.

Main Results:

  • HCMV, unlike HSV-1 and VACV, induces proteasomal degradation of LMAN2L during early infection.
  • HCMV protein pUS2 mediates LMAN2L degradation via ER-associated protein degradation (ERAD) pathway recruitment of RNF139 and UBE2G2.
  • LMAN2L knockout impairs HCMV-induced type I interferon and interferon-stimulated gene expression.
  • LMAN2L is essential for STING translocation from the ER to the Golgi, but not for STING dimerization or TBK1 recruitment.

Conclusions:

  • LMAN2L is a novel host regulator of the STING pathway.
  • HCMV utilizes pUS2-mediated ERAD to degrade LMAN2L, representing a previously unrecognized viral immune evasion strategy.