Main Menu

Influenza virus is a major public health concern, causing up to 500,000 deaths annually. The current strategy of reformulating vaccines annually against dominant circulating strains leads to variable protective efficacy and is unlikely to protect against novel influenza viruses with pandemic potential. Thus, there is a great need for a vaccine that provides “universal” protection against influenza viruses.

A highly efficient method to genetically modify natural killer (NK) cells to induce expression of high affinity CD16 (HA-CD16) through mRNA electroporation, to potentiate NK cell-mediated antibody-dependent cellular cytotoxicity (ADCC). ADCC is mediated by CD16+ NK cells following adoptive NK cell transfer, but most humans express CD16 which has a relatively low affinity for IgG1 antibodies.

The invention relates to compounds that inhibit HIV-1 DNA synthesis mediated by reverse transcriptase (RT). HIV-1 DNA synthesis by RT utilizes deoxynucleoside 5’-triphosphate (dNTP) as substrate and like many other enzymes, the reaction is reversible. Pyrophosphate analogs like imidodiphosphate strongly promote reverse reaction dNTP products containing the imidodiphosphate group instead of the naturally occurring pyrophosphate group. This imidodiphosphate-containing dNTP was found to be a potent inhibitor of the forward RT reaction.

Noroviruses are now recognized as the major cause of non-bacterial gastroenteritis in all age groups, and efforts are underway to develop an effective vaccine. The lack of a robust cell culture system for human noroviruses has complicated vaccine development. Hence, norovirus virus like particles (VLPs) have played an important role in the understanding of virus structure, immune response, antigenic diversity, and vaccine design.

With respect to quantification of metabolites in the brain, conventional methods of magnetic resonance spectroscopy (MRS) yield results that are highly variable and highly dependent on the sequence type being applied. This invention describes a novel MRS technique that involves preparing longitudinal steady states at different flip angles using trains of RF pulses interspersed with field gradients to quantify metabolites.

Streptococcus pneumoniae (S. pneumonia), bacteria commonly referred to as pneumococcus, are a significant cause of disease resulting in 1.5 million deaths every year worldwide according to the World Health Organization. The major types of pneumococcal disease are pneumonia (lung infection), bacteremia (bloodstream infection), and meningitis (infection of the tissue covering of the brain and spinal cord). Less severe pneumococcal illnesses include ear and sinus infections.

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.