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Liudi Tang, PhD

Assistant Professor

Education & Professional Training

B.A., Biotechnology, China Pharmaceutical University, 2012

M.S., Microbiology and Biochemical Pharmacy, China Pharmaceutical University, 2014

Ph.D., Microbiology & Immunology, Drexel University College of Medicine, 2019

Post-doctorate, Virology, Evrys Bio, 2022

Research Summary

My career interest is to understand the viral-host interactions that determine hepatitis B virus (HBV) persistent infection, particularly focusing on its early life cycle including viral nucleocapsid trafficking, uncoating, and the establishment of covalently closed circular (ccc) DNA. In addition, my laboratory also focuses on developing novel gene editing technologies aiming at selectively destroy HBV-infected hepatocytes to potentially cure chronic Hepatitis B, a disease that affects more than 250 million people and claims appropriately 1 million lives per year.

Current Research Projects

  1. Selective targeting HBV-infected hepatocytes through novel gene therapies. We are developing a first-in-class HBV RNA-sensing and ADAR-editing dependent protein expression system (HBV-RADARS). Briefly, a UAG stop codon surrounded by a short stretch of anti-HBV sequence is designed to terminate protein translation from the HBV-RADARS RNA, unless it hybridizes with HBV RNA to form a double-stranded RNA duplex with an A-C mismatch bubble, which subsequently recruits the cellular RNA editing enzyme adenosine deaminase acting on RNA (ADAR) to conduct the A-to-I editing (UAG to UIG), after which the stop codon is converted into a translational readthrough codon. Therefore, versatile reporter proteins can be produced strictly in cells that contain HBV RNA.
  2. Investigate the interplay between HBV X protein and host SMC5/6 in regulating viral transcription dynamics. Our group is also interested in the role of HBx as a viral factor critical for HBV transcription. HBx interacts with DDB1 and serves as a viral DCAF (DDB1- and CUL4-associated factor) to direct the Cullin 4 – RING E3 ubiquitin ligase to degrade the structural maintenance of chromosomes (SMC) SMC5/6 complex, which otherwise recognizes and restricts transcription from episomal DNA such as HBV cccDNA and other viruses with extrachromosomal circular DNA genome. Our study continues to decipher the intricate regulation of HBx metabolism and episomal DNA transcription dynamics under different physiological conditions, which will shed light on HBx-targeting drug discovery aiming to achieve long-term SMC5/6 mediated control of HBV.

Publications

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View on National Library of Medicine.

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