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This invention describes a method for vaccination against Ebola virus. Outbreaks of hemorrhagic fever caused by the Ebola virus, particularly the Zaire subtype, are associated with high mortality rates. The virus is very contagious, and during an outbreak, presents a threat to anybody who comes into contact with an infected person. Because the virus progresses so rapidly and the mortality rate is so high, there is little opportunity to develop natural immunity, making vaccination a promising intervention.

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.

West Nile virus (WNV) has recently emerged in the U.S. and is considered a significant emerging disease that has embedded itself over a considerable region of the U.S. WNV infections have been recorded in humans as well as in different animals. From 1999-2014, WNV killed 1,765 people in the U.S. and caused severe disease in more than 41,762 others. This project is part of NIAID's comprehensive emerging infectious disease program.

A human mast cell line LAD2 that more closely resembles normal in vivo and in vitro human mast cells by expressing functional FcepsilonRI receptors and responding to stem cell factor (SCF) with proliferation, as described in Leuk Res. 2003 Aug;27(8):677-82 and developed by the laboratory of Dr. Dean Metcalfe at the National Institute of Allergy and Infectious Diseases.  This cell line also releases mediators by cross-linking FcgammaRI (CD64) receptors and express FcgammaRII (CD32).

The invention relates to a dengue virus tetravalent vaccine containing a common 30-nucleotide deletion (delta30) in the 3'-untranslated region (UTR) of the genome of dengue virus serotypes 1, 2, 3, and 4. The previously identified delta30 attenuating mutation, created in dengue virus type 4 (DEN4) by the removal of 30 nucleotides from the 3'-UTR, is also capable of attenuating a wild-type strain of dengue virus type 1 (DEN1).

An expression vector with a unique promoter that results in higher level of protein expression than vectors currently in use is available for licensing from the NIH. The elevated levels of expression are achieved through use of a specific promoter, known as CMV/R, in which the Human T-Lymphotrophic Virus (HTLV-1) Long Terminal Repeat (LTR) R-U5 region is substituted for a portion of the intron downstream of the CMV immediate early region 1 enhancer (Barouch et al., 2005). Sequences of 95% or better homology to CMV/R can be used as well.

This invention relates to a VAC-BAC shuttle vector system for the creation of recombinant poxviruses from DNA cloned in a bacterial artificial chromosome. A VAC-BAC is a bacterial artificial chromosome (BAC) containing a vaccinia virus genome (VAC) that can replicate in bacteria and produce infectious virus in mammalian cells.

This invention identifies a monoclonal antibody (4G10) against the chemokine receptor CXCR4 and is a mouse IgG1 antibody. CXCR4 has been identified as a co-receptor mediating entry of HIV-1 into T cells. Subsequently, CXCR4 has been implicated in normal physiological functions, including activation of B cells and B cell progenitors and guiding their migration into the bone marrow (via its ligand SDF-1). CXCR4 also functions in T cell progenitor migration and neural progenitor stem cell activation.

This invention provides a novel family of acylthiols and uses thereof. More specifically, this invention provides effective inhibitors of HIV that selectively target its highly conserved nucleocapsid protein (NCp7) by interacting with metal chelating structures of a zinc finger-containing protein. Because of the mutationally intolerant nature of NCp7, drug resistance is much less likely to occur with compounds attacking this target.

NF-kB has been found to be important in immune responses, cell proliferation, apoptosis, and in organ development. Several years ago it was discovered that an IKKgamma/NEMO protein was essential as an adaptor molecule to mediate TNF-alpha, IL-1, and oncoprotein induced activation of NF-kB. Mutation in IKKgamma/NEMO also results in two human genetic diseases, Familial incontinentia pigmenti and hypohidrotic/anhidrotic ectodermal dysplasia. The NIH announces mouse monoclonal antibodies to IKKgamma/NEMO that are far superior to other immunological reagents.