Phosphodiesterase-induced cAMP degradation restricts hepatitis B virus infection

• DOI: 10.1098/rstb.2018.0292
• Publication Date: 2019-04-08T07:06:13Z
• Authors: Antonia Alexandra...; Ana Maria Ortega-...; Jessica Katy Skelton; Quentin Bazot; Marcus Dorner
• Keywords: Life Sciences & Biomedicine - Other Topics; 0301 basic medicine; Hepatitis B virus; sodium taurocholate cotransporting polypeptide; 610; Organic Anion Transporters, Sodium-Dependent; CELL-MIGRATION; POLYPEPTIDE; Hepatitis; 03 medical and health sciences; Virus de la hepatitis; Virology; BINDING; Cyclic AMP; Humans; Dimethyl Sulfoxide; phosphodiesterases; PHOSPHORYLATION; Biology; 11 Medical and Health Sciences; Evolutionary Biology; Science & Technology; Symporters; Phosphoric Diester Hydrolases; TRANSPORTER; Articles; Hep G2 Cells; 06 Biological Sciences; Virología - Investigación; Hepatitis B; Virus; 3. Good health; Hepatitis - Tratamiento; Gene Expression Regulation, Neoplastic; ENTRY; viral entry; Life Sciences & Biomedicine; hepatitis B virus

Hepatitis B virus (HBV) entry into hepatocytes is mediated via a high-affinity interaction between the preS1 glycoprotein and sodium/bile acid cotransporting polypeptide (NTCP). To date, in vitro model systems rely on high multiplicities of infection to achieve cell lines overexpressing human NTCP. This study investigates novel regulatory pathway for NTCP trafficking surface, induced by DMSO-mediated cellular differentiation. DMSO rapidly induces surface expression results increased susceptibility cells HBV infection. Additionally, treatment actin, as well Tubulin reshaping within cells. We show that direct disruption actin network directly enhances subsequent these changes alterations levels cyclic (c)AMP, which participates observed rearrangements. Blocking phosphodiesterases (PDEs), degrade accumulated cAMP, had same effect differentiation demonstrates prevents phosphodiesterase-mediated cAMP degradation. identifies adenylate cyclase target blocking targeting accumulation article part theme issue ‘Silent cancer agents: multi-disciplinary modelling DNA oncoviruses’.