Current therapies for chronic hepatitis B virus (HBV) infection can effectively suppress viral replication but do not achieve a functional or complete cure. Capsid assembly modulators inhibit the assembly of viral capsids, prevent the encapsidation of pregenomic RNA, and interfere with both the formation and amplification of covalently closed circular DNA, which is essential for viral persistence.

Traditional neoantigen prediction methods primarily rely on HLA-peptide binding databases, often producing false positives. This challenge highlights the need for improved strategies to identify truly immunogenic neoantigens. Neoantigen-based cancer vaccines have shown promising efficacy in recent clinical trials for treating solid tumors, offering a potential solution.

Both IL-15 and IL-2 are good options for cancer therapy, but IL-15 is considered superior due to lower vascular endothelial toxicity, stronger ability to expand natural killer and CD8+ T cells and weaker stimulation of T regulatory cells, but it has a short half-life and exerts severe adverse effects.

Immunity is not a function most people particularly associate with the liver. But because of its connection to the gut, the liver is exposed to bacterial metabolites as few other organs are. And when either the liver or the gut is not functioning well, it can adversely affect immunity as well. The liver is connected to the gut via both the biliary system and the portal vein. Those two conduits allow metabolites from the gut microbiome to influence what’s going on in the liver. Both liver and gut damage can affect this communication for the worse. And surprisingly, one of the consequences is immune dysfunction.

Drug resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors, occurring via secondary mutations or bypass pathways, is frequent among non-small-cell lung cancer patients.