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TLR9: an important molecule in the fight against hepatitis B virus
  1. Aziz Shahrakyvahed1,
  2. Javad Sanchooli2,
  3. Nima Sanadgol3,4,
  4. Mohammad Kazemi Arababadi5,
  5. Derek Kennedy6
  1. 1Department of Nursing, Faculty of Nursing and Midwifery, Zabol University of Medical Sciences, Zabol, Iran
  2. 2Department of Immunology, Faculty of Medicine, Zabol University of Medical Sciences, Zabol, Iran
  3. 3Department of Biology, Faculty of Science, University of Zabol, Zabol, Iran
  4. 4Faculty of Pharmacy and Pharmaceutical Science Research Center (PSRC), Tehran University of Medical Sciences (TUMS), Tehran, Iran
  5. 5Immunology of Infectious Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
  6. 6School of Natural Sciences, Eskitis Institute for Drug Discovery, Griffith University Nathan, Queensland, Australia
  1. Correspondence to Dr Mohammad Kazemi Arababadi, Immunology of Infectious Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan 7718665179, Iran; dr.kazemi{at}


Hepatitis B virus (HBV) is the most prevalent infectious agent that can induce severe liver disease. Patients infected with long-term HBV, including chronic, asymptomatic and occult forms, cannot clear HBV from infected hepatocytes completely. It is not clear why some people can clear the infection while others cannot. Furthermore, the main mechanisms responsible for progression of the infections are not fully understood. It has been hypothesised that differences in genetic and immunological parameters between patients and subjects who successfully clear HBV infections are responsible for inducing the long-term forms of the infection. Previous investigations showed that Toll-like receptors (TLRs) play important roles in immune responses, especially innate immunity, against viral infections, including hepatitis B. TLR9 detects intracellular viral dsDNA, which results in the activation of an immune response against HBV. However, defects in this system may result in an attenuated response ultimately leading to long-term HBV infections. Targeting the defects in TLR9 or reactivating the downstream pathways that are normally switched on by TLR9 in response to HBV infection is a new approach to the treatment of long-term HBV infection. However, the pathways and defects seen in patients with long-term HBV need to be thoroughly explored before therapeutics can be applied in the clinical setting. Furthermore, the apparently multigenic nature of long-term HBV infection suggests that treatment of patients may need to be personalised.

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