Abstract <p>Hepatitis B virus (HBV) infects human hepatocytes, causing acute or chronic liver infection. Chronic HBV infection leads to progressive liver damage, potentially resulting in cirrhosis or hepatocellular carcinoma. One promising antiviral strategy involves activating cytidine deaminases of the APOBEC/AID family, which could induce mutational degradation of HBV. Using a CRISPRa-based transcriptional activation system with modified sgRNAs, we investigated antiviral and oncogenic effects of the activating genes encoding APOBEC3C, APOBEC3D, and APOBEC3H.</p>

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Antiviral and Mutagenic Effects of APOBEC Deaminases A3C, A3D, and A3H in a Hepatitis B Virus Model

  • Ivan V. Karandashov,
  • Sergey A. Brezgin,
  • Natalia I. Ponomareva,
  • Andrey S. Tikhonov,
  • Vladimir P. Chulanov,
  • Dmitry S. Kostyushev,
  • Anastasiya P. Kostyusheva

摘要

Abstract

Hepatitis B virus (HBV) infects human hepatocytes, causing acute or chronic liver infection. Chronic HBV infection leads to progressive liver damage, potentially resulting in cirrhosis or hepatocellular carcinoma. One promising antiviral strategy involves activating cytidine deaminases of the APOBEC/AID family, which could induce mutational degradation of HBV. Using a CRISPRa-based transcriptional activation system with modified sgRNAs, we investigated antiviral and oncogenic effects of the activating genes encoding APOBEC3C, APOBEC3D, and APOBEC3H.