Harvard College

Duke University

Dana-Farber-Cancer Institute Inc.

Immune Disease Institute, Inc.

David M Knipe

George Rainer Siber

Judy Lieberman

Bryan R Cullen

Donald M Coen

Neal A DeLuca

Robert W Finberg

Deborah Palliser

Megan Horn Orzalli

Igor Jurak

Jennifer Lin Umbach

Elizabeth E McNamee

Travis J Taylor

Martha F Kramer

Kai Xia

A method for augmenting expression of a heterologous nucleic acid in a eukaryotic cell or increasing the efficiency of gene expression using any gene expression system is carried out by decreasing expression or activity of an endogenous Interferon-induced protein-16 (IFI16).

Foreign DNA surveillance protein

The present invention relates, in general, to micro RN As and, in particular, to viral microRNAs expressed by Herpes Simplex Vims 1 (HSV-1) or Herpes Simplex Virus 2 (HSV-2), to agents that inhibit such microRNAs and to methods of treatment based on the use of such agents.

Viral microRNA

The invention provides a microbicidal composition comprising at least one siRNA. The siRNA is an RNA duplex made of one or two molecules. A portion of the siRNA is identical to a target sequence in an essential gene of a virus. The virus may be a herpesvirus, for example, HSV-1 or HSV-2. Preferably, the herpesvirus is HSV-2. The microbicidal composition further comprises a pharmaceutically acceptable carrier. Also included in the invention are methods to prevent and treat viral infections by administration of the microbicidal composition. Preferably, the microbicidal composition is administered transmucosally.

siRNA microbicides for preventing and treating diseases

A herpesvirus vaccine comprising a mutated herpesvirus suspended in a pharmaceutically acceptable carrier. The mutated herpesvirus is capable of infecting cells of the mammal to be vaccinated, but incapable of completing a replicative cycle, and it is capable of eliciting a protective immune response in that mammal. The mutated herpesvirus is also capable of treating immunomodulatory or immunoregulatory diseases. The mutation occurs in at least one gene encoding a protein essential for replication of the virus, so that the mutation renders the virus replication defective.

Herpesvirus replication defective mutants

The claimed invention embodies a replication competent virus that expresses a detectable fusion protein. Any viral protein can be used to construct the fusion protein and fused with a detectable protein, such as a fluorescent protein. The claimed invention also relates to method for screening viral resistant cells and methods for identifying anti-viral agents or agents the block expression of the viral protein.

Replication-competent virus expressing a detectable fusion protein

The present invention relates to a method of identifying a compound which modulates (enhances, inhibits, reduces) herpesvirus infection of a vertebrate cell comprising the steps of combining a phosphorylating enzyme capable of catalyzing the phosphorylation of ICP4, a substrate comprising a polypeptide which is phosphorylated by the enzyme, a phosphate source and the compound to be assessed; maintaining the combination under conditions appropriate for phosphorylation of the substrate; and determining phosphorylation of the substrate which occurs in the presence of the compound to be assessed. The present invention also relates to the compounds identified by the methods of the present invention.

Method of identifying compounds which modulate herpesvirus infection

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Auburndale, MA, United States of America

David M Knipe