Article Text
Statistics from Altmetric.com
Chronic hepatitis B virus (HBV) infection remains a significant global health burden, affecting over 250 million people worldwide who are at risk of developing liver cirrhosis and hepatocellular carcinoma (HCC). Currently available nucleos(t)ide analogues (NAs) are effective in controlling viraemia; however, functional cure, defined as loss of hepatitis B surface antigen (HBsAg), is rare and difficult to achieve and likely requires robust immune responses, reflecting the need for innovative therapeutic strategies.1 Thus, the future of treating chronic HBV infections relies on combination therapies that include both direct-acting antiviral agents and immunomodulatory agents.2 In this context, selgantolimod (SLGN), an agonist of Toll-like receptor 8 (TLR8), could be a promising candidate. Its efficacy in the treatment of chronic HBV infections has been investigated in preclinical models and clinical trials,3–5 but there remains limited understanding of its impact on immune effectors within the liver. The study by Roca Suarez and colleagues published in Gut 6 aimed to bridge that knowledge gap by characterising the transcriptomic changes and intercellular communication events induced by SLGN in the hepatic microenvironment and investigating its effect on HBV–host interactions.
The researchers of Fabien Zoulim’s laboratory identified TLR8-expressing cell types in the …
Footnotes
Contributors TB and MC wrote the manuscript. MU-Q designed the graphical abstract. All authors provided critical review of the manuscript.
Funding Funding provided by the European Union (ERC-AdG-2020-FIBCAN #101021417 (TB), HORIZON-HLTH-2021-DISEASE-04-07 D-SOLVE #101057917 (TB and MC)), the French government (ANR-10-IAHU-02, ANR-10-LABX-0028, ANR-21-RHUS-0001, TB), the German Center for Infection Research (DZIF; TTU‐05‐701, TTU‐05‐702, TTU-IICH-07-808, MC) and the Excellence Cluster RESIST (EXC2155, MC).
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.