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Host-specific ubiquitination of prM orchestrates ESCRT recruitment to mediate efficient Japanese Encephalitis Virus

Chenxi Li1,2,3,4, Wenzhuang Guo1, Wen Zhao5

  • 1College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China.

Plos Pathogens
|July 8, 2026
PubMed

Insights

Mosquito-borne viruses like Japanese encephalitis virus (JEV) hijack host systems. This study reveals JEV prM protein ubiquitination in vertebrates, crucial for viral budding and host adaptation.

Area of Science:

  • Virology
  • Molecular Biology
  • Host-Pathogen Interactions

Background:

  • Mosquito-borne orthoflaviviruses (e.g., JEV, DENV, ZIKV) are significant global health threats.
  • These viruses manipulate host ubiquitin systems for replication and pathogenesis.
  • The specific roles of viral protein ubiquitination in orthoflavivirus infection are not fully understood.

Purpose of the Study:

  • To investigate the molecular mechanisms of viral protein ubiquitination in Japanese encephalitis virus (JEV) infection.
  • To identify specific viral targets and understand their functional significance in host adaptation and viral life cycle.
  • To elucidate the role of ubiquitination in the differential adaptation of orthoflaviviruses between vertebrate hosts and mosquito vectors.

Main Methods:

  • Identification of JEV prM protein as a target for host-specific ubiquitination.
  • Analysis of ubiquitination sites (lysine residues K107/108/116) conserved across multiple orthoflaviviruses.
  • Investigation of the interaction between ubiquitinated prM and the ESCRT machinery, including TSG101.

Main Results:

  • JEV prM protein undergoes ubiquitination exclusively in vertebrate hosts, not in mosquitoes.
  • Ubiquitination at conserved lysine residues in prM of various orthoflaviviruses influences host-vector adaptation.
  • prM ubiquitination recruits TSG101 and other ESCRT components, facilitating viral particle budding.

Conclusions:

  • Viral protein ubiquitination is a key mechanism regulating JEV infection and host adaptation.
  • The ESCRT pathway, recruited via ubiquitinated prM, plays a critical role in viral budding.
  • These findings offer insights into the adaptive evolution of orthoflaviviruses across diverse hosts and vectors.

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