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Due to the disorganized nature of blood vessels that run through tumors, chemotherapeutic agents often fail to penetrate tumors and kill cancer cells at the tumor’s center. This can lead to ineffective chemotherapeutic treatments, because tumors can quickly grow back if the entire tumor is not destroyed. NIH researchers have developed a therapeutic agent that solves this problem facing current chemotherapy treatments.

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.

The invention is an imaging agent and method of use for imaging blood pools and the lymphatic system. The imaging agent binds with high affinity to serum albumin, the most abundant serum protein, and can be tagged with several isotopes making it suitable for magnetic resonance imaging or positron emission tomographic imaging. To date, only very few blood-pool tracers have been introduced for positron emission tomography. The existing ones have short half-lives (20.4 min for ¹¹C and 2.05 min for ¹⁵O) and thus can only be used in centers with an in-house cyclotron.

A plasmid encodes human interleukin-8 (IL-8) receptor CXCR1. IL-8 is a chemo-attractant cytokine that attracts and activates neutrophils in inflammatory regions.

Rotavirus is a highly contagious, diarrhea-inducing pathogen that annually causes approximately 250,000 deaths worldwide and millions of hospitalizations, especially afflicting infants and young children. One strategy to combat this virus is through vaccination. Continuing safety and efficacy concerns with the currently existing live, oral vaccines against rotavirus have led researchers to search for alternative treatment approaches, such as vaccines containing inactivated rotavirus.

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.

CDC researchers have developed probes and primers for detecting the 2009 pandemic influenza A H1N1 virus in patient samples using real-time reverse transcription-polymerase chain reaction (rRT-PCR) methods. These primers and probes were originally developed in 2009 and were cleared by the FDA as part of a domestic human diagnostic testing panel in June 2010. These were also updated to increase specificity and/or sensitivity of the detection methods.

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.

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.