The present invention discloses a method for assessing the capacity of a substance to treat or prevent hepadnavirus infection. A reporter virus carrying genetic information for a first fragment of a recombinase and a reporter cell expressing a second fragment of the recombinase are used. When the reporter virus infects the reporter cell, the two fragments of the recombinase associate and excise a stop cassette that is flanked by two recombination sites and blocks the expression of a reporter gene. Accordingly, the present invention relates to a method of assessing the capacity of a substance to treat or prevent hepadnavirus infection, a hepadnavirus comprising a nucleic acid encoding a first fragment of a recombinase and a mammalian hepatocyte or hepatoma cell comprising a nucleic acid encoding a second fragment of a recombinase and a nucleic acid comprising a stop cassette flanked by two recombination sites fused to a reporter gene.

The invention provides a novel fusion protein between flagellin (or portions thereof) and a polypeptide that can form a virus-like particle (VLP) (e.g., hepatitis b core (HBc) protein or portions thereof), where the fusion protein continues to form a VLP in an aqueous environment. The VLPs based on such fusion proteins (e.g., FH VLPs) provide a versatile, highly immunogenic, and safe vaccine carrier capable of displaying or associating a variety of vaccine antigens on VLP surface to elicit potent humoral and cellular immune responses.

An evaluation system for replication activity of HBV capable of visualizing and quantifying replication of HBV DNA in a short period of time inexpensively, safely, and rapidly and a method for evaluation using the system are developed and provided. Moreover, a novel composition for inhibiting HBV replication with a mode of action different from that of conventional anti-HBV drugs is developed and provided. A therapeutic agent for hepatitis B comprising as an active ingredient an HBV-Pol activity inhibitor consisting of a phosphorylation inhibitor that inhibits phosphorylation of a TxY motif present in Terminal protein region of HBV-Pol is provided.

Described herein are compositions and methods for treating a subject having or at risk of developing a neurocognitive disorder, such as Alzheimer's disease or Nasu-Hakola disease. For example, using the compositions and methods of the disclosure, a subject having or at risk of developing a neurocognitive disorder may be administered one or more cells that contain a transgene encoding triggering receptor expressed on myeloid cells two (TREM2), such as a population of CD34+ hematopoietic stem or progenitor cells that express TREM2, thereby treating or preventing the disorder.

Described herein are methods for treating a subject having or at risk of developing a neurocognitive disorder, such as frontotemporal lobar degeneration or neuronal ceroid lipofuscinosis, by administering cells that contain a transgene encoding a progranulin (PGRN) or a granulin (GRN) or cells that express the PGRN or the GRN to the subject. Also disclosed are compositions comprising cells containing the transgene encoding the PGRN or the GRN.

The present invention discloses a method for assessing the capacity of a substance to treat or prevent hepadnavirus infection. A reporter virus carrying genetic information for a first fragment of a recombinase and a reporter cell expressing a second fragment of the recombinase are used. When the reporter virus infects the reporter cell, the two fragments of the recombinase associate and excise a stop cassette that is flanked by two recombination sites and blocks the expression of a reporter gene. Accordingly, the present invention relates to a method of assessing the capacity of a substance to treat or prevent hepadnavirus infection, a hepadnavirus comprising a nucleic acid encoding a first fragment of a recombinase and a mammalian hepatocyte or hepatoma cell comprising a nucleic acid encoding a second fragment of a recombinase and a nucleic acid comprising a stop cassette flanked by two recombination sites fused to a reporter gene.

The present invention provides a therapeutic or prophylactic agent for cancer, containing an expression vector encoding a chimeric Hepatitis B virus core antigen polypeptide inserted with an amino acid sequence containing a specific epitope of VEGF and/or a specific epitope of angiopoietin-2, wherein the amino acid sequence containing the specific epitope is inserted between the amino acid residues 80 and 81 of the hepatitis B virus core antigen polypeptide.

The present invention relates to tumor immunotherapy, in particular to tumor vaccination, using chimeric proteins comprising all or a portion of a hepatitis B virus core antigen protein and an amino acid sequence comprising an epitope derived from the extracellular portion of a tumor-associated antigen. In particular, the present invention provides virus-like particles comprising said chimeric proteins, which are useful for eliciting a humoral immune response in a subject against the tumor-associated antigen, in particular against cells carrying said tumor-associated antigen on their surface, wherein the tumor-associated antigen is a self-protein in said subject.

Methods and compositions are provided for the treatment of glaucoma and other optic neuropathies.

The present invention provides compositions and methods for rescuing FANCA expression in cells with diminished or no FANCA gene product. In particular, methods and compositions for gene therapy of Fanconi anemia are disclosed.