Abstract
Hepatitis B virus (HBV), an enveloped partially double-stranded DNA virus, is a widespread human pathogen responsible for more than 250 million chronic infections worldwide. Current therapeutic strategies cannot eradicate HBV due to the persistence of the viral genome in a special DNA structure (covalently closed circular DNA, cccDNA). The identification of sodium taurocholate co-transporting polypeptide (NTCP) as an entry receptor for both HBV and its satellite virus hepatitis delta virus (HDV) has led to great advances in our understanding of the life cycle of HBV, including the early steps of infection in particular. However, the mechanisms of HBV internalization and the host factors involved in this uptake remain unclear. Improvements in our understanding of HBV entry would facilitate the design of new therapeutic approaches targeting this stage and preventing the de novo infection of naïve hepatocytes. In this review, we provide an overview of current knowledge about the process of HBV internalization into cells.
Highlights
Inserm U1259, Morphogénèse et Antigénicité du VIH et des Virus des Hépatites (MAVIVH), Plate-Forme IBiSA des Microscopies, PPF ASB, Université de Tours and CHRU de Tours, 37032 Tours, France
Expression is rapidly lost after the isolation of primary human hepatocytes [71]. These observations may explain why malignant hepatoma cells do not support infection with Hepatitis B virus (HBV) and hepatitis delta virus (HDV), and why primary hepatocytes are susceptible to HBV for only a few days after isolation
The identification of NTCP as a specific entry receptor for HBV and HDV was a major breakthrough that has greatly advanced our understanding of HBV life cycle
Summary
Viruses are small organisms with a simple structure and composition Their interactions with host cells are complex and not always fully understood. Viruses generally bind to cell-surface proteins before interacting with specific receptors, leading to the activation of cellular signaling pathways. Some viruses, such as human immunodeficiency virus 1. Caveolin-mediated endocytosis occurs within microdomains of the plasma membrane known as lipid rafts. These microdomains are enriched in cholesterol and sphingolipids, together with lipid-raft specific proteins: caveolins and cavins [6]. Entry into the lumen of endosomes or macropinosomes is accompanied by a change in environment, leading to changes in the viral particle resulting in the activation of the virus and its passage across the vacuolar membrane to deliver the viral genome or capsid into the cytosol
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