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H7N9 influenza viruses are predominately avian (bird) pathogens, however, since 2013, they have infected more than 1500 humans with a mortality rate of nearly 40% in confirmed cases. H7N9 viruses continue to be a threat to public health. Treatment for people infected with H7N9-subtype influenza A (H7N9) commonly includes the use of drugs that inhibit neuraminidase, a protein found on the virus’ surface. However, like other influenza viruses, H7N9 can become resistant to these drugs.

The molecular imaging technique of positron emission tomography (PET) is an increasingly important tool in biomedical research and in drug discovery and development. Many small molecule drugs and potential PET radiotracers carry trifluoromethyl (CF₃) groups. Because CF₃ groups are generally considered to be metabolically stable, there is a strong interest in developing drugs with these groups.

Streptococcus pneumoniae is the leading cause of community-acquired pneumonia and is also a frequent cause of bloodstream, brain and spinal cord, ear, and sinus infections. According to 2015 CDC data, an estimated 900,000 Americans get pneumococcal pneumonia each year and approximately 5-7% die from it annually. Accurate diagnosis and early treatment are important for improving patient outcomes.

This technology is directed towards a potential treatment for a new disease, CHAPLE (Complement Hyperactivation, Angiopathic thrombosis, and Protein-Losing Enteropathy), identified by NIAID researchers. CHAPLE is associated with GI symptoms and vascular thrombosis and is caused by loss-of-function variants in the gene encoding the complement regulatory protein CD55. The disease is caused by enhanced activation of the complement pathway and complement-mediated induction of intestinal lymphangiectasia and protein-losing enteropathy.

Multiple sclerosis (MS) is an autoimmune disease caused by activated autoimmune T lymphocytes in patients resulting in inflammatory demyelination in the central nervous system. Current treatments are focused on functional control of these activated autoimmune T cells, but these treatments are non-specific T cell inhibitors and have serious, sometimes fatal side effects. A specific therapy aimed at eliminating these autoimmune T cells through restimulation-induced cell death (RICD) could cure the disease and overcome the fatal side effects of current therapies.

The technology addresses treatment options for diseases such as sickle-cell and thalassemia. Traditionally, such beta-globinopathies are treated through bone marrow transplantation. However, this method is limited due to high treatment costs and finding a matched-donor. This relies on increasing fetal hemoglobin to potentially cure the disease. NIH inventors have identified a protein called Rio-Kinase 3 (RIOK3), that inhibits the production of fetal hemoglobin. Their work shows that inhibiting RIOK3 increases the production of fetal hemoglobin.

Clinical and biological specimens often contain microbial nucleic acid in extremely low quantities, presenting a significant challenge for the detection of viral and bacterial pathogens. This also prevents direct sequencing of non-culturable samples using next-generation sequencing (NGS). Currently, NGS library preparation on most platforms requires 0.1 ng to 10 µg of DNA or cDNA, while microbial or viral nucleic acids in clinically relevant specimens, such as blood, serum, respiratory secretions, cerebral spinal fluid, and stool, often contain less than 0.1 ng.

These small molecules are novel nucleotide derivatives, containing either a purine or pyrimidine nucleobase, that competitively block the enzyme CD73, also known as ecto-5'-nucleotidase. This enzyme converts extracellular AMP (not a potent activator of adenosine receptors) to adenosine (the native activator of 4 subtypes of adenosine receptors. CD73 inhibitors are being used, in clinical trials and preclinical research, in conjunction with cancer immunotherapy.

IRF8, a member of interferon regulatory factor (IRF) family of transcription factors is a novel intrinsic transcriptional inhibitor of TH17-cell differentiation. TH17-cells are believed to be involved in the pathogenesis of various autoimmune/inflammatory diseases. These materials could be used to help define patterns of gene expression important for the development and function of cells including possible contributions to understanding: normal immune responses, inflammatory conditions, autoimmunity and anti-viral responses.

There is a great need for broadly protective, “universal” influenza virus vaccines given the antigenic drift and shift of influenza viruses and the variable protective efficacy of the current influenza vaccines. This technology relates to a broadly protective, “universal” influenza vaccine candidate composed of a cocktail of different low pathogenicity avian influenza virus subtypes inactivated by betapropiolactone (BPL).