Abstract: The present invention relates to a method able to enhance survival and functionality of anti-tumor or anti-viral immune cells through overexpression of Akt molecules in the cells. Akt signaling prevented the expression of immune checkpoints and therefore rescued antigen-specific cytotoxic T lymphocytes from exhaustion in immunosuppressive microenvironment.

Abstract: In a first aspect, the present invention relates to the use of a TLR 9 agonist and/or a TLR 4 agonist in a prophylactic or therapeutic vaccine. According to the present vaccination strategy, the TLR 9 agonist and/or TLR 4 agonist is adapted or designed for use as a multiplying jump agent to enhance numbers and functionality of CD8 T cells in a prime-jump vaccination strategy for jump T cell expansion. In particular, the TLR 9 agonist and/or TLR 4 agonist is used as a component to be administered after priming of the individual to be vaccinated. The vaccination strategy is particularly useful against acute and chronic infections with intracellular pathogens or for anti-tumor vaccination. In another aspect, the present invention relates to a kit of part containing a prime agent and a multiplying jump agent according to the present invention.

Abstract: The present invention is directed to a use of a heat shock protein inhibitor in preparing pharmaceutical composition for treating hepatitis by scavenging hepatitis B virus-infected cells. The heat shock protein inhibitor is selected from a group including VER-155008, Pifithrin-?, and pharmaceutical acceptable salts thereof. The present invention is also directed to a use of a heat shock protein inhibitor in preparing pharmaceutical composition for treating hepatoma.

Abstract: In a first aspect, the present invention relates to the use of a TLR 9 agonist and/or a TLR 4 agonist in a prophylactic or therapeutic vaccine. According to the present vaccination strategy, the TLR 9 agonist and/or TLR 4 agonist is adapted or designed for use as a multiplying jump agent to enhance numbers and functionality of CD8 T cells in a prime-jump vaccination strategy for jump T cell expansion. In particular, the TLR 9 agonist and/or TLR 4 agonist is used as a component to be administered after priming of the individual to be vaccinated. The vaccination strategy is particularly useful against acute and chronic infections with intracellular pathogens or for anti-tumor vaccination. In another aspect, the present invention relates to a kit of part containing a prime agent and a multiplying jump agent according to the present invention.

Abstract: The present invention is directed to a use of a heat shock protein inhibitor in preparing pharmaceutical composition for treating hepatitis by scavenging hepatitis B virus-infected cells. The heat shock protein inhibitor is selected from a group including VER-155008, Pifithrin-?, and pharmaceutical acceptable salts thereof. The present invention is also directed to a use of a heat shock protein inhibitor in preparing pharmaceutical composition for treating hepatoma.

Abstract: Disclosed is a recombinant plasmid for expressing hepatitis B viral antigens in vivo, comprising an adeno-associated virus (AVV) vector and a replication-competent hepatitis B virus genome fragment. Mice hydrodynamically injected with the recombinant plasmid of the present invention show persistent expression of hepatitis B viral antigens for more than 6 months in the hepatocytes, thus a immuno-competent mouse model for persistent expression of hepatitis B antigens and also for human chronic hepatitis B virus infection is established, which can be applied in evaluation and elucidation of mechanism of chronic hepatitis and anti-viral drug discovery research.

Abstract: Disclosed is a recombinant plasmid for expressing hepatitis B viral antigens in vivo, comprising an adeno-associated virus (AVV) vector and a replication-competent hepatitis B virus genome fragment. Mice hydrodynamically injected with the recombinant plasmid of the present invention show persistent expression of hepatitis B viral antigens for more than 6 months in the hepatocytes, thus a immuno-competent mouse model for persistent expression of hepatitis B antigens and also for human chronic hepatitis B virus infection is established, which can be applied in evaluation and elucidation of mechanism of chronic hepatitis and anti-viral drug discovery research.