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  • team
  • department
  • center
  • program_project
  • nrc
  • whocc
  • project
  • software
  • tool
  • patent
  • Administrative Staff
  • Assistant Professor
  • Associate Professor
  • Clinical Research Assistant
  • Clinical Research Nurse
  • Clinician Researcher
  • Department Manager
  • Dual-education Student
  • Full Professor
  • Honorary Professor
  • Lab assistant
  • Master Student
  • Non-permanent Researcher
  • Nursing Staff
  • Permanent Researcher
  • Pharmacist
  • PhD Student
  • Physician
  • Post-doc
  • Prize
  • Project Manager
  • Research Associate
  • Research Engineer
  • Retired scientist
  • Technician
  • Undergraduate Student
  • Veterinary
  • Visiting Scientist
  • Deputy Director of Center
  • Deputy Director of Department
  • Deputy Director of National Reference Center
  • Deputy Head of Facility
  • Director of Center
  • Director of Department
  • Director of Institute
  • Director of National Reference Center
  • Group Leader
  • Head of Facility
  • Head of Operations
  • Head of Structure
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Published in The Journal of infectious diseases - 07 Jan 2025

Suspène R, Caval V, Khalfi P, Pitré E, Marchio A, Pineau P, Vartanian JP

Link to Pubmed [PMID] – 39761821

Link to DOI – 10.1093/infdis/jiaf002

J Infect Dis 2025 Jan; ():

Restriction factors are host cell proteins that play a role in limiting virus replication. They form part of the intrinsic immune system and function as a first line of defense against viral infections. Hepatitis B virus (HBV) does not escape this rule and TREX1, a host restriction enzyme acts as an antiviral factor, leading to the inhibition of the virus.TREX1-expressing constructs were generated and modified by site-directed mutagenesis. The location and activity of the different TREX1 constructs were analyzed by Immunofluorescence and FACS. HepaD38 cells were either transfected or transduced with the different TREX1 constructs in presence or absence of cobalt chloride-mimicked hypoxia and released HBV was quantified by qPCR.We identified TREX1 as a restriction factor that suppresses HBV replication. Furthermore, TREX1 expression was increased in the presence of cobalt chloride, a chemical agent mimicking hypoxia. Thus, by treating cells with cobalt chloride, TREX1 reduced HBV replication by a factor of 2, demonstrating that under hypoxic conditions, TREX1 restricts HBV replication. Finally, an analysis of 36 HBV-infected patients with hepatocellular carcinoma revealed that TREX1 expression was inversely correlated to the HBV viral and HBV cccDNA.Current treatments are unable to eliminate HBV genomic reservoirs, which persist as covalently closed episomal circular DNA. TREX1 is a novel restriction factor that blocks HBV replication. It would be therapeutically relevant to study whether HBV nucleocapsid recycling containing TREX1 enzyme could be released into the nucleus and degrade the viral and nuclear DNA of infected cells.