The present invention concerns the use of a protein comprising at least a HIV-derived accessory protein tat (trans-activator of transcription) or any derivative thereof for the reactivation of latent human immunodeficiency virus (HIV) from cells present in a HIV-infected patient.

The disclosure provides helix grafted proteins, methods of producing helix grafted proteins and methods of use of helix grafted proteins as inhibitors of protein-protein interactions involved in disease pathogenesis.

Disclosed are novel fusion protein constructs comprising a functional mitochondrial protein, that can enter mitochondria within intact cells. Further disclosed are methods of treating mitochondrial disorders by the disclosed fusion proteins and compositions therefor.

In some aspects, the present invention cell-penetrating compstatin analog and compositions comprising cell-penetrating compstatin analog. In some aspects, the invention further provides methods of using cell-penetrating compstatin analogs treat a complement-mediated disorder, e.g., to inhibit complement-mediated damage to a cell, tissue, or organ, to inhibit production or release of biologically active C3 cleavage products.

The present invention has a function of enabling the penetration of the blood-brain barrier and the blood-spinal cord barrier of the central nervous system, which have not been significantly penetrated, with excellent efficiency, thereby enabling a rapid, quick, and more efficient therapeutic effect to be obtained through low dose administration. In addition, the present invention enables local administration unlike conventional therapeutic agents, thereby decreasing side effects, and enables local administration of a therapeutic agent at a high concentration, thereby enabling potentially new treatments and prescriptions.

Disclosed are fusion protein constructs comprising a functional mitochondrial protein, that can enter mitochondria within intact cells. Further disclosed are methods of treating mitochondrial disorders by the disclosed fusion proteins and compositions therefor.

A method of reducing a latent HIV-specific memory-CD4+ T cell pool in a subject includes the steps of: preparing at least one HIV-1 protein coding sequence from a sample obtained from the subject, wherein the sample includes HIV-1 RNA; introducing the at least one HIV-1 protein coding sequence into at least one expression construct using yeast homologous recombination; transfecting a cell with the at least one expression construct, wherein the HIV-1 protein is secreted by the cell and administering a therapeutically effective amount of the secreted HIV-1 protein and a pharmaceutically acceptable carrier to the subject, wherein the secreted HIV-1 protein stimulates latent HIV-specific memory-CD4+ T cells to induce latent HIV-1 replication resulting in HIV-specific memory-CD4+ T cell death in the subject.

A chimeric vector is provided in the present invention, which is formed by ligating a Vif protein and a functional protein, the functional protein being a Raf protein or a Rev protein. By designing and constructing a Rev-Vif-C vector and then demonstrating that the Rev-Vif-C vector has a good anti-virus effect by a variety of experiments, the present invention proposes a novel anti-virus technology against the Rev protein of HIV-1. Moreover, by designing and constructing a RBD-Vif-C vector and then demonstrating that the RBD-Vif-C vector has a good tumor cell killing effect by cell-level experiments in vitro and experiments in vivo with nude mouse tumor models, the present invention proposes a novel anti-tumor technology specifically against mutant KRAS.

This disclosure relates to the genetic modification of DNMT3A gene in immune cells. In certain embodiments, the modified immune cells may be used in adoptive T cells therapies to enhance immune responses against cancer or chronic infections. In certain embodiments, the disclosure relates to deleting, changing, or inserting nucleotides within the DNMT3A gene in immune cells, e.g., human CD8 T cells, such that the DNMT3A gene product does not function for methylation. In certain embodiments, modification of the DNMT3A gene provides an improvement in antigen-specific T cells functions and/or an enhancement of the longevity of the cells.

C-Terminal Fragments of Glucagon-Like Peptide-1 (GLP 1), and methods of use thereof, e.g., for the treatment of obesity and obesity-related disorders, e.g., diabetes and the metabolic syndrome.