[1] Hsu YC, Huang DQ, Nguyen MH. Global burden of hepatitis B virus: current status, missed opportunities and a call for action. Nat Rev Gastroenterol Hepato, 2023. [2] Hyams KC. Risks of chronicity following acute hepatitis B virus infection: a review. Clin Infect Dis, 1995, 20(4):992-1000. [3] McMahon BJ. Natural History of Chronic Hepatitis B. Clin Liver Dis, 2010, 14(3):381-396. [4] Thomas DL. Global Elimination of Chronic Hepatitis. N Engl J Med, 2019, 380(21):2041-2050. [5] Sheena BS, Hiebert L, Han H, et al. Global, regional, and national burden of hepatitis B, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet Gastroenterol Hepatol, 2022, 7(9):796-829. [6] Yuen MF, Chen DS, Dusheiko GM, et al. Hepatitis B virus infection. Nat Rev Dis Primers, 2018, 4(1):1-20. [7] Jeng WJ, Papatheodoridis GV, Lok ASF. Hepatitis B. Lancet, 2023, 401(10381):1039-1052. [8] Hossain MG, Akter S, Ohsaki E. Impact of the Interaction of Hepatitis B Virus with Mitochondria and Associated Proteins. Viruses, 2020, 12(2):175. [9] Loureiro D, Tout I, Narguet S, et al. Mitochondrial stress in advanced fibrosis and cirrhosis associated with chronic hepatitis B, chronic hepatitis C, or nonalcoholic steatohepatitis. Hepatology, 2023, 77(4):1348-1365. [10] Liang YJ, Teng W, Chen CL, et al. Clinical Implications of HBV PreS/S Mutations and the Effects of PreS2 Deletion on Mitochondria, Liver Fibrosis, and Cancer Development. Hepatology, 2021, 74(2):641-655. [11] Wheelhouse NM, Lai PBS, Wigmore SJ. Mitochondrial D-loop mutations and deletion profiles of cancerous and noncancerous liver tissue in hepatitis B virus-infected liver. Br J Cancer. 2005;92(7):1268-1272. [12] Fujita N, Sugimoto R, Ma N, et al. Comparison of hepatic oxidative DNA damage in patients with chronic hepatitis B and C. J Viral Hepat, 2008, 15(7):498-507. [13] Yang D, Oyaizu Y, Oyaizu H, Olsen GJ, Woese CR. Mitochondrial origins. Proc Natl Acad Sci U S A, 1985, 82(13):4443-4447. [14] Anderson S, Bankier AT, Barrell BG, et al. Sequence and organization of the human mitochondrial genome. Nature, 1981, 290(5806):457-465. [15] Suliman HB, Piantadosi CA. Mitochondrial Quality Control as a Therapeutic Target. Pharmacol Rev, 2016, 68(1):20-48. [16] Spinelli JB, Haigis MC. The multifaceted contributions of mitochondria to cellular metabolism. Nat Cell Biol, 2018, 20(7):745-754. [17] Vyas S, Zaganjor E, Haigis MC. Mitochondria and Cancer. Cell, 2016, 166(3):555-566. [18] Marchi S, Guilbaud E, Tait SWG. Mitochondrial control of inflammation. Nat Rev Immunol, 2023, 23(3):159-173. [19] An P, Wei LL, Zhao S, et al. Hepatocyte mitochondria-derived danger signals directly activate hepatic stellate cells and drive progression of liver fibrosis. Nat Commun, 2020, 11(1):2362. [20] Mitchell C, Robin MA, Mayeuf A, et al. Protection against hepatocyte mitochondrial dysfunction delays fibrosis progression in mice. Am J Pathol, 2009, 175(5):1929-1937. [21] Zhao Y, Wang Z, Feng D, et al. p66Shc Contributes to Liver Fibrosis through the Regulation of Mitochondrial Reactive Oxygen Species. Theranostics, 2019, 9(5):1510-1522. [22] Zhang L, Zhang Y, Chang X, et al. Imbalance in mitochondrial dynamics induced by low PGC-1α expression contributes to hepatocyte EMT and liver fibrosis. Cell Death Dis, 2020, 11(4):226. [23] Wang J, Yang Y, Sun F, et al. ALKBH5 attenuates mitochondrial fission and ameliorates liver fibrosis by reducing Drp1 methylation. Pharmacol Res, 2023, 187:106608. [24] Okamoto H, Tsuda F, Sakugawa H, et al. Typing hepatitis B virus by homology in nucleotide sequence: comparison of surface antigen subtypes. J Gen Virol, 1988, 69 ( Pt 10):2575-2583. [25] Takada S, Shirakata Y, Kaneniwa N, et al. Association of hepatitis B virus X protein with mitochondria causes mitochondrial aggregation at the nuclear periphery, leading to cell death. Oncogene, 1999, 18(50):6965-6973. [26] Rahmani Z, Huh KW, Lasher R, et al. Hepatitis B virus X protein colocalizes to mitochondria with a human voltage-dependent anion channel, HVDAC3, and alters its transmembrane potential. J Virol, 2000, 74(6):2840-2846. [27] Bouchard MJ, Wang LH, Schneider RJ. Calcium signaling by HBx protein in hepatitis B virus DNA replication. Science, 2001, 294(5550):2376-2378. [28] Waris G, Huh KW, Siddiqui A. Mitochondrially associated hepatitis B virus X protein constitutively activates transcription factors STAT-3 and NF-kappa B via oxidative stress. Mol Cell Biol, 2001, 21(22):7721-7730. [29] Shirakata Y, Koike K. Hepatitis B virus X protein induces cell death by causing loss of mitochondrial membrane potential. J Biol Chem, 2003, 278(24):22071-22078. [30] Lee YI, Hwang JM, Im JH, et al. Human hepatitis B virus-X protein alters mitochondrial function and physiology in human liver cells. J Biol Chem, 2004, 279(15):15460-15471. [31] Gao WY, Li D, Cai DE, et al. Hepatitis B virus X protein sensitizes HL-7702 cells to oxidative stress-induced apoptosis through modulation of the mitochondrial permeability transition pore. Oncol Rep, 2017, 37(1):48-56. [32] Clippinger AJ, Bouchard MJ. Hepatitis B virus HBx protein localizes to mitochondria in primary rat hepatocytes and modulates mitochondrial membrane potential. J Virol, 2008, 82(14):6798-6811. [33] Ling LR, Zheng DH, Zhang ZY, et al. Effect of HBx on inflammation and mitochondrial oxidative stress in mouse hepatocytes. Oncol Lett, 2020, 19(4):2861-2869. [34] Geng X, Huang C, Qin Y, et al. Hepatitis B virus X protein targets Bcl-2 proteins to increase intracellular calcium, required for virus replication and cell death induction. Proc Natl Acad Sci U S A, 2012, 109(45):18471-18476. [35] Kim SJ, Khan M, Quan J, Till A, Subramani S, Siddiqui A. Hepatitis B virus disrupts mitochondrial dynamics: induces fission and mitophagy to attenuate apoptosis. PLoS Pathog, 2013, 9(12):e1003722. [36] Chi HC, Chen SL, Lin SL, et al. Thyroid hormone protects hepatocytes from HBx-induced carcinogenesis by enhancing mitochondrial turnover. Oncogene, 2017, 36(37):5274-5284. [37] Fisicaro P, Barili V, Montanini B, et al. Targeting mitochondrial dysfunction can restore antiviral activity of exhausted HBV-specific CD8 T cells in chronic hepatitis B. Nat Med, 2017, 23(3):327-336. [38] Acerbi G, Montali I, Ferrigno GD, et al. Functional reconstitution of HBV-specific CD8 T cells by in vitro polyphenol treatment in chronic hepatitis B. J Hepatol, 2021, 74(4):783-793. [39] Lee SY, Choi YM, Oh SJ, et al. rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections. Front Immunol, 2019, 10:1735. [40] Huang C, Shao J, Lou C, et al. Reduced Energy Metabolism Impairs T Cell-Dependent B Cell Responses in Patients With Advanced HBV-Related Cirrhosis. Front Immunol, 2021, 12:660312. [41] Chen T, Xun Z, Lin J, et al. Association between mitochondrial DNA content and baseline serum levels of HBsAg in chronic hepatitis B infection. J Med Virol, 2017, 89(11):1958-1962. [42] Li L, Hann HW, Wan S, et al. Cell-free circulating mitochondrial DNA content and risk of hepatocellular carcinoma in patients with chronic HBV infection. Sci Rep, 2016, 6:23992. |