Abstract: Compositions and methods for the prevention and/or treatment of a viral infection, in particular of the Coronaviridae family.

Abstract: Compositions and methods for the prevention and/or treatment of a viral infection, in particular of the Coronaviridae family.

Abstract: The present invention relates to chimeric protein kinase molecules and methods for designing inhibitors of protein kinases using the chimeric protein kinases of the present invention. The chimeric protein kinase of the present invention comprise inhibitor binding site residues of a non-crystallizable protein and non-inhibitor binding site residues of a crystallizable protein. The chimeric protein is preferably crystallizable and is useful for designing inhibitors for the non-crystallizable protein. In addition, the present invention is directed to a protein kinase inhibitor binding site which is outside the ATP binding site of the protein kinase and methods of use therefore.

Abstract: Transdominant HIV tat substitution and truncated gene mutants of 72 amino acid residues or less are disclosed. The mutated genes encode mutant Tat proteins which are capable of inhibiting the expression of the HIV-1 virus in the presence of an equimolar concentration of the wild type Tat protein in vitro. Therapeutic agents which include fused protein forms of the mutant proteins are also disclosed, as well as methods of preparing and using the therapeutic agents in the treatment of HIV infection and HIV-related injections in an animal. Recombinant vectors which express the mutant HIV Tat proteins described are also disclosed, as well as cell lines which product high yields of the mutant HIV. Also provided are cell lines that express enhanced levels of TAR mutant viruses relative to other TAR mutant infected cell lines. Levels of production are enhanced by the use of cell lines that express a transactivator protein, such as adenovirus transactivator EIA and/or EIB protein.

Abstract: Compositions including a polypeptide or nucleic acid sequence encoding a polypeptide that binds TAR DNA (particularly the region -18 to +28 of HIV-LTR DNA) and that does not bind to TAR RNA (particularly the region +1 to +80 of the TAR RNA) are disclosed. The cellular binding protein TDP-43 including the polypeptide has an estimated molecular weight of between about 40 kD and 46 kD as determined by SDS polyacrylamide gel electrophoresis. Fusion proteins that include the entire cellular binding protein TDP-43 or fragments thereof are also described. The cellular binding protein, peptide fragments and nucleic acid sequences encoding them, repress HIV gene expression. Methods for preparing the cellular binding protein from cells as recombinant proteins with recombinant host cells are also disclosed. Antibodies to the TDP-43 cellular binding protein are also described. The isolated nucleic acid sequences of the protein and its fragments are described in the construction of retroviral vectors.

Abstract: Transdominant HIV tat substitution and truncated gene mutants of 72 amino acid residues or less are disclosed. The mutated genes encode mutant Tat proteins which are capable of inhibiting the expression of the HIV-1 virus in the presence of an equimolar concentration of the wild type Tat protein in vitro. Therapeutic agents which include fused protein forms of the mutant proteins are also disclosed, as well as methods of preparing and using the therapeutic agents in the treatment of HIV infection and HIV-related injections in an animal. Recombinant vectors which express the mutant HIV Tat proteins described are also disclosed, as well as cell lines which product high yields of the mutant HIV.

Abstract: The invention relates to a cellular protein which is specific and has high affinity for nucleic acid sequences characteristic of an intact TAR RNA loop sequence of the HIV LTR TAR region. The invention also relates to a protein preparation having a protein of about 185 kD that is isolated from a mammalian cell nuclear extract preparation, most specifically a HeLa cell extract that is purified between 1,000-10,000 fold. The protein of about 185 kD is shown to regulate HIV viral gene expression by binding a TAR RNA region of an HIV LTR template, in the presence of a cofactor fraction (including at least a -100 kD cofactor), and a tat protein. A route for the development of immunodiagnostics for AIDS and related disorders may also be provided given the specific and high affinity of TRP-185 for HIV RNA.

Abstract: Transdominant HIV tat substitution and truncated gene mutants of 72 amino acid residues or less are disclosed. The mutated genes encode mutant Tat proteins which are capable of inhibiting the expression of the HIV-1 virus in the presence of an equimolar concentration of the wild type Tat protein in vitro. Therapeutic agents which include fused protein forms of the mutant proteins are also disclosed, as well as methods of preparing and using the therapeutic agents in the treatment of HIV infection and HIV-related injections in an animal. Recombinant vectors which express the mutant HIV Tat proteins described are also disclosed, as well as cell lines which product high yields of the mutant HIV.

Abstract: A gene encoding a cellular factor that binds to NFAT-like elements in the HIV-LTR has been obtained by .lambda.gt11 expression cloning using oligonucleotides corresponding to these binding motifs. This cDNA encodes a ubiquitously expressed 60 kD protein, termed interleukin binding factor (ILF), which binds specifically to such purine rich motifs in the HIV-LTR. ILF also binds to similar purine-rich motifs in the IL-2 promoter, although with lower affinity than to HIV-LTR sequences. Sequence analysis reveals the ILF DNA binding domain to have strong homology with the recently described fork head DNA binding domain of the Drosophila homeotic protein, fork head, and a family of hepatocyte-nuclear factors, HNF-3. Other domains found in ILF include a nucleotide binding site, an N-glycosylation motif, a signal for ubiquitin-mediated degradation, and a potential nuclear localization signal.

Abstract: The invention relates to a cellular protein which is specific and has high affinity for nucleic acid sequences characteristic of an intact TAR RNA loop sequence of the HIV LTR TAR region. The invention also relates to a between 1,000-10,000-fold purified, about 185 kD protein preparation isolated from a mammalian cell nuclear extract preparation, most specifically a HeLa cell extract. The about 185 kD protein is shown to regulate HIV viral gene expression by binding a TAR RNA region of an HIV LTR template, in the presence of a cofactor fraction (including at least a.about.100 kD cofactor), and a tat protein. The TRP-185, having a molecular weight of about 185 kD protein may also provide a research tool in the study of viral and cellular gene expression. A route for the development of immunodiagnostics for AIDS and related disorders may also be provided given the specific and high affinity of TRP-185 for HIV RNA.