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Two side roads toward conquest of HBV

Hepatitis B virus are not an enclosed (like its ring-shaped DNA) mystery any more. Two kinds of intervention, GDC-0449 namely receptor antagonists and histone deacetylase inhibitors, can be theoretically used.

The first side-road is to stop the entry of HBV.

One Chinese group first found and proved sodium taurocholate cotransporting polypeptide (NTCP) as a probable host receptor for HBV. This coincide with HBV patients' aberrant cholesterol metabolism. More experiments shall be done with NTCP antagonists such as Myrcludex-B (a synthetic N-acylated preS1 lipopeptide) and Cyclosporin Paclitaxel A (usage restricted by its immunosuppressant role).

The second side-road is to interfere with HBV DNA/RNA replication within host cell nuclear.
Popular HDAC1,2, and even Ezh1, Ezh2, Suv12 complex assemble at HBV's cccDNA, regarding it as a mini-chromosome. This is believed to explain HBV's consistent infection without integration and protection from clearance by immune cells. One can even suspect that increased level of HDAC1 or hSirt1 in many HCC tissues may be HBV's tricks.

We strongly hope that some combinations of the candidates can crack down HBV.

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