Researchers at the Department of Gastroenterology, Hepatology, Infectiology and Endocrinology at Hannover Medical School (MHH), being part of the D-SOLVE consortium, have identified a marker on natural killer cells influenced by the drug bulevirtide. Hepatitis D viruses (HDV) cause severe chronic hepatitis. Bulevirtide, available in Europe since mid-2023, blocks the docking point for viral envelopes on liver cells and alleviates liver inflammation early in treatment. The MHH team, led by Clinic Director Professor Dr. Heiner Wedemeyer and Dr. Norman Woller, discovered that natural killer cells (NK cells) play a crucial role in this process. The findings were published in the scientific journal ‘Hepatology’ (please follow the link to the original paper).

HDV requires the hepatitis B virus (HBV) to infect liver cells. Hepatitis D infection only occurs with hepatitis B and exacerbates the existing infection. Hepatitis D is rare but aggressive, affecting 10 to 20 million people worldwide and can quickly lead to liver cirrhosis or cancer.

The research team analyzed the immune system of chronic hepatitis D (CHD) patients treated with bulevirtide. They focused on NK cells, which are the first line of defense against virus-infected cells and cancer. Significant changes were detected in a marker called TIGIT on NK cells, important for immune response, during therapy. TIGIT acts as a brake to prevent excessive inflammatory reactions. During bulevirtide treatment, TIGIT activation increased, while levels of alanine aminotransferase, a marker for liver inflammation, decreased. This was not observed in control groups of chronic hepatitis C and B patients.

Clarifying bulevirtide’s influence on the TIGIT signaling pathway could help develop new drugs against liver inflammation.