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Praziquantel has been the drug of choice for the treatment of schistosomiasis for over 40 years. However, it is effective only against adult worms, and the reliance on a single drug increases the risk that resistance will develop. New antischistosomals targeting multiple stages of the worms’ life cycle are needed. Dr. Conor Caffrey, Professor at the Center for Discovery and Innovation in Parasitic Diseases (CDIPD) and the Skaggs School of Pharmacy & Pharmaceutical Sciences at University of California, San Diego, will investigate natural product derivatives synthesized by Dr. Peter Cheuka, Lecturer and Researcher in Medicinal Chemistry and Drug Discovery at University of Zambia. The compounds will be tested against various developmental stages of Schistosoma mansoni at CDIPD to determine bioactivity and identify interesting scaffolds for further development.

Chagas disease, human African trypanosomiasis (HAT), and leishmaniasis are among the infectious diseases that disproportionately exact a heavy toll on people living in low- and middle-income countries. Dr. Marcelo Comini, Head of the Redox Biology of Trypanosomes Laboratory at the Institut Pasteur de Montevideo, works on the discovery of novel drugs targeting the pathogens responsible for these diseases. The Seattle Structural Genomics Center for Infectious Disease, which is contracted through the United States National Institute of Allergy and Infectious Diseases (contract HHSN272201700059C), will investigate the crystal structure of three proteins identified by Dr. Comini to inform rational design of new treatments for Chagas disease, HAT, and leishmaniasis.

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This application relates to immunogenic conjugates which elicit an immune response to Plasmodium proteins. This application claims conjugates that include at least one Plasmodium sexual stage surface protein covalently linked to at least one Plasmodium circumsporozoite protein (CSP) or an immunogenic portion of a CSP. Also claimed are conjugates that include at least one sexual stage surface protein covalently linked to at least one immunogenic repeat derived from a Plasmodium CSP. The inventors' data shows that these conjugates also induced long-lasting antibody responses to each of their components, i.e. the vaccine candidates showed both transmission blocking activity and antibodies to the CSP (or portion thereof). The inventors have previously shown that P. falciparum conjugates of the ookinete surface protein Pfs25 are immunogenic and induce long-lasting IgG antibody responses in mice. The inventors have also previously shown that adsorption of the conjugates onto aluminum hydroxide further increased the antibody response. Remarkably, the antibody levels three or seven months after the last injection were significantly higher than those one week after that injection. Such a vaccine would block disease transmission if most/all the population is immunized. Plasmodium falciparum causes the most severe form of malaria; one to three percent of the parasites are highly virulent, causing the death of approximately two million people annually, ninety percent of whom are young children. Plasmodium vivax is the most widespread cause of malaria. There is as yet no licensed prophylactic vaccine for this disease. Furthermore, malarial parasites are increasingly becoming resistant to antimalarial drugs that have been used to treat the disease for decades.
Anti-Arthropod Vector Vaccines, Methods of Selecting, and Uses Thereof; NIH Internal Reference E-122-2001/0 More information is available here: Leishmania parasites are transmitted to their vertebrate hosts by infected phlebotomine sand fly bites. Sand fly saliva is known to enhance Leishmania infection, while immunity to the saliva protects against infection. This invention claims nine major salivary proteins from the sand fly vector of Leishmania major, Phlebotomus papatasi, nucleic acids encoding the proteins, vaccines comprising the proteins and/or nucleic acids, and methods of producing an immune response to prevent Leshmaniasis. The inventors have shown that one of these salivary proteins was able to protect vaccinated mice challenged with parasites plus salivary gland homogenates SGH . A DNA vaccine containing the cDNA for the same protein provided this same protection. Protection lasted at least 3 months after immunization. The vaccine produced both intense humoral and delayed-type hypersensitivity DTH reactions. B cell-deficient mice immunized with the plasmid vaccine successfully controlled Leishmania infection when injected with Leishmania plus SGH.