Abstract: Provided herein is the use of compounds that modulate the activity of inhibitor of apoptosis proteins (IAPs), alone or in combination with other therapeutic agents, in the treatment of human immunodeficiency virus (HIV).

Abstract: Provided herein is the use of compounds that modulate the activity of inhibitor of apoptosis proteins (IAPs), alone or in combination with other therapeutic agents, in the treatment of human immunodeficiency virus (HIV).

Abstract: Provided herein is the use of compounds that modulate the activity of inhibitor of apoptosis proteins (IAPs), alone or in combination with other therapeutic agents, in the treatment of human immunodeficiency virus (HIV). Described herein is the use of IAP antagonists in the treatment of human immunodeficiency virus (HIV) in a mammal, alone or in combination with other therapeutic agents used in HIV therapy. In one aspect, provided herein is a method of treating human immunodeficiency virus (HIV) in an individual in need thereof comprising administering a therapeutically effective amount of at least one inhibitor of apoptosis proteins (IAP) antagonist.

Abstract: Provided herein is the use of compounds that modulate the activity of inhibitor of apoptosis proteins (1APs), alone or in combination with other therapeutic agents, in the treatment of human immunodeficiency virus (HIV). Described herein is the use of IAP antagonists in the treatment of human immunodeficiency virus (HIV) in a mammal, alone or in combination with other therapeutic agents used in HIV therapy. In one aspect, provided herein is a method of treating human immunodeficiency virus (HIV) in an individual in need thereof comprising administering a therapeutically effective amount of at least one inhibitor of apoptosis proteins (IAP) antagonist.

Abstract: This disclosure concerns antimicrobial compositions and methods for immunoenhancement, for example methods of increasing production of a type I interferon (IFN) in response to pathogen infection, by administration of a TAM receptor inhibitor. In certain embodiments, the disclosure concerns methods of using a TAM receptor inhibitor to treat a viral or bacterial infection in a subject.

Abstract: This disclosure concerns antimicrobial compositions and methods for immunoenhancement, for example methods of increasing production of a type I interferon (IFN) in response to pathogen infection, by administration of a TAM receptor inhibitor. In certain embodiments, the disclosure concerns methods of using a TAM receptor inhibitor to treat a viral or bacterial infection in a subject.

Abstract: This disclosure concerns antimicrobial compositions and methods for immunoenhancement, for example methods of increasing production of a type I interferon (IFN) in response to pathogen infection, by administration of a TAM receptor inhibitor. In certain embodiments, the disclosure concerns methods of using a TAM receptor inhibitor to treat a viral or bacterial infection in a subject.

Abstract: Disclosed herein are methods of expressing a heterologous nucleic acid sequence, such as a sequence encoding a detectable protein, in a primary neuron (or plurality of primary neurons) and other neurons that are monosynaptically connected to the primary neuron (or plurality of primary neurons). Such methods involve viruses (such as, rabies viruses) defective for transsynaptic transport (TST-defective virus) and in situ complementation of the defect in a manner that permits only monosynaptic transport of the TST-defective virus. The TST-defective virus and, therefore, any heterologous nucleic acid sequence it carries in its genome, are not transmitted to neurons that are not monosynaptically connected to the primary neuron (or plurality of primary neurons). Also disclosed are methods of targeting a TST-defective virus to a genetically defined primary neuron (or plurality of primary neurons).

Abstract: A method of screening test chemicals or compounds as inhibitors of HIV replication is disclosed. In one embodiment, the method comprises the step of determining whether the test chemical or compound is a sulfonation inhibitor. In another embodiment, the invention is a method of treating an HIV infected individual to reduce HIV replication comprising the step of treating the individual with an effective amount of sulfonation inhibitor.

Abstract: Disclosed herein are methods of expressing a heterologous nucleic acid sequence, such as a sequence encoding a detectable protein, in a primary neuron (or plurality of primary neurons) and other neurons that are monosynaptically connected to the primary neuron (or plurality of primary neurons). Such methods involve viruses (such as, rabies viruses) defective for transsynaptic transport (TST-defective virus) and in situ complementation of the defect in a manner that permits only monosynaptic transport of the TST-defective virus. The TST-defective virus and, therefore, any heterologous nucleic acid sequence it carries in its genome, are not transmitted to neurons that are not monosynaptically connected to the primary neuron (or plurality of primary neurons). Also disclosed are methods of targeting a TST-defective virus to a genetically defined primary neuron (or plurality of primary neurons).

Abstract: Disclosed herein are antiviral agents, in particular non-nucleoside reverse transcriptase inhibitors (NNRTIs) of the formula Also disclosed are methods of making the NNRTIs, as well as compositions that include such NNRTIs and methods of their use for treating viral infections, in particular retroviral infections, such as HIV infection.

Abstract: This disclosure concerns antimicrobial compositions and methods for immunoenhancement, for example methods of increasing production of a type I interferon (IFN) in response to pathogen infection, by administration of a TAM receptor inhibitor. In certain embodiments, the disclosure concerns methods of using a TAM receptor inhibitor to treat a viral or bacterial infection in a subject.

Abstract: Disclosed herein are methods of expressing a heterologous nucleic acid sequence, such as a sequence encoding a detectable protein, in a primary neuron (or plurality of primary neurons) and other neurons that are monosynaptically connected to the primary neuron (or plurality of primary neurons). Such methods involve viruses (such as, rabies viruses) defective for transsynaptic transport (TST-defective virus) and in situ complementation of the defect in a manner that permits only monosynaptic transport of the TST-defective virus. The TST-defective virus and, therefore, any heterologous nucleic acid sequence it carries in its genome, are not transmitted to neurons that are not monosynaptically connected to the primary neuron (or plurality of primary neurons). Also disclosed are methods of targeting a TST-defective virus to a genetically defined primary neuron (or plurality of primary neurons).

Abstract: A cell-free viral uncoating assay is provided.

Abstract: The present invention relates to mammalian anthrax toxin receptor polypeptides and polynucleotides encoding same as well as related polypeptides and polynucleotides, vectors containing the polynucleotides and polypeptides, host cells containing related polynucleotide molecules, and cells displaying no anthrax toxin receptor on an exterior surface of the cells—minus cell lines and animals. The present invention also relates to methods for identifying molecules that bind the anthrax toxin receptor and molecules that reduce the toxicity of anthrax toxin. Finally, the present invention provides methods for treating human and non-human animals suffering from anthrax.

Abstract: Disclosed herein are methods of expressing a heterologous nucleic acid sequence, such as a sequence encoding a detectable protein, in a primary neuron (or plurality of primary neurons) and other neurons that are monosynaptically connected to the primary neuron (or plurality of primary neurons). Such methods involve viruses (such as, rabies viruses) defective for transsynaptic transport (TST-defective virus) and in situ complementation of the defect in a manner that permits only monosynaptic transport of the TST-defective virus. The TST-defective virus and, therefore, any heterologous nucleic acid sequence it carries in its genome, are not transmitted to neurons that are not monosynaptically connected to the primary neuron (or plurality of primary neurons). Also disclosed are methods of targeting a TST-defective virus to a genetically defined primary neuron (or plurality of primary neurons).

Abstract: The present invention relates to mammalian anthrax toxin receptor polypeptides and polynucleotides encoding same as well as related polypeptides and polynucleotides, vectors containing the polynucleotides and polypeptides, host cells containing related polynucleotide molecules, and cells displaying no anthrax toxin receptor on an exterior surface of the cells-minus cell lines and animals. The present invention also relates to methods for identifying molecules that bind the anthrax toxin receptor and molecules that reduce the toxicity of anthrax toxin. Finally, the present invention provides methods for treating human and non-human animals suffering from anthrax.

Abstract: Novel targeting methods of viral entry are disclosed herein.

Abstract: The present invention concerns the discovery of a new member of the TNF receptor superfamily, referred to herein as the candidate "tvb receptor". Experimental evidence suggests that the instant gene corresponds to the gene of the tvb.sup.s3 locus responsible for mediating certain viral infection. The tvb receptor plays a functional role as the receptor for certain of the avian leukosis/sarcoma viruses (ALSV) in avians, and a likely role as a receptor for tumor viruses in other animals, e.g., the feline leukemia virus and the like. Moreover, inspection of the tvb sequence, particularly in comparison with other TNF receptors, reveals the presence of a "death domain" in the cytoplasmic tail of the tvb receptor, suggesting a role for the tvb receptor in determining tissue fate and maintenance. For instance, the tvb genes and gene products may participate, under various circumstances, in the control of proliferation, differentiation and/or cell death.