The Salk Institute for Biological Studies

Wisconsin Alumni Research Foundation

Harvard College

Sanford Burnham Prebys Medical Discovery Institute

John A T Young

R John Collier

Nicholas David Peter Cosford

Mitchell Dennis Vamos

Greg Erwin Lemke

John M Marlett

Sumit K Chanda

Peter Teriete

Kenneth A Bradley

Carla V Rothlin

Lars Pache

Suchita Bhattacharyya

Ian R Wickersham

Edward M Callaway

Arturo Diaz

Jeremy S Mogridge

Shakti Narayan

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).

Use of inhibitor of apoptosis protein (IAP) antagonists in HIV therapy

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.

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.

Use of TAM receptor inhibitors as antimicrobials

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). The disclosed technology enables far more specific labelling and/or manipulation of neural networks than has previously been possible.

Compositions and methods for monosynaptic transport

A cell-free viral uncoating assay is provided.

Assay to detect viral uncoating

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&#x2014;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.

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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.

Growing community of inventors

San Diego, CA, United States of America

John A T Young