CD46 regulates Hepatitis B infection 

( 12.24.25  )                                    Written by Gio Kim          

Hepatitis B virus (HBV) remains a global health threat to this day. With over 296 million people living with chronic HBV infection and with 1.5 million new cases reported annually, chronic HBV infection can lead to severe complications, including cirrhosis and hepatocellular carcinoma, which are liver diseases.

The virus enters the cell using a receptor called NTCP (sodium taurocholate co-transporting polypeptide), but not much information is known about what regulates NTCP’s presence on the cell’s surface.

In this study, researchers found that removing CD46, a membrane cofactor protein, from cells caused a significant reduction of NTCP on the surface of the cell, which strongly reduced HBV infection. They also tested antibodies against CD46, particularly the clone E4.3, and discovered that these antibodies could actively trigger NTCP to internalize into intracellular vesicles. This prevented the HBV from entering the cell using NTCP. More importantly, scientists confirmed these effects not only in lab grown liver cells but in primary human hepatocytes (a type of cell that makes up 60% of the liver).

This discovery reveals a previously unknown mechanism controlling HBV entry into cells. While medications exist for HBV, targeting CD46 could become a promising strategy to prevent or treat Hepatitis B infections.

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You can read the full paper here:

https://academic.oup.com/jmcb/advance-article/doi/10.1093/jmcb/mjaf055/8402925