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The technology offered for licensing is foundational in the area of recombinant DNA vaccines. In the last several years, facilitated through a licensing program of the NIH, the technology has been broadly applied in the development and commercialization of several novel human and veterinary vaccines in the areas of infectious disease as well as cancer therapeutics. The NIH wishes to expand its licensing program of the subject technology in a variety of applications that will benefit public health.

Offered for licensing is a recombinant attenuated vaccinia virus, MVA, that expresses the haemagglutinin (HA) and nucleoprotein (NP) of influenza virus A/PR/8/34 (H1N1). The virus has been shown to stimulate protective immunity to influenza virus in mice.

The materials can be used for research purposes and in particular in the area of influenza virus vaccines.

The related publications listed below demonstrate the usefulness of this biological material in influenza virus vaccine research.

Offered for licensing is a recombinant attenuated vaccinia virus, MVA, that expresses SIV 239gagpol. The materials can be used for research purposes and in particular in the area of HIV/AIDS vaccines.

The technology offered for licensing is in the field of vaccinia-based recombinant vaccines. In particular the invention relates to methods of stabilizing the recombinant virus, thus resulting in efficient production of the vaccine and efficient expression of the inserted gene. Stabilization of the recombinant virus is achieved by the insertion of the exogenous gene into an intergenic region (IGR) of the viral genome (i.e. Modified Vaccinia Ankara, MVA), where the IGR is flanked by open reading frames of conserved poxvirus genes.

One of the major limitations of using cultured keratinocytes for research studies is that primary keratinocytes senesce after a few passages. Keratinocytes from specific anatomical sites are also difficult to culture. Scientists at the NIH have demonstrated that primary keratinocytes, from several anatomical sites, when treated with a small-molecule inhibitor of the ROCK protein maintain a proliferative state and become immortal without genetic modification to the cells.

Investigators at the NIH have discovered a potential means for preventing or treating a herpes virus infection by inhibiting the activity of the host cell’s histone demethylases. When herpesviruses enter a cell, they are inactivated by cellular defense mechanisms that wrap the viral genome in repressive chromatin structures. In order for viral replication to progress, the host’s own histone demethylases are recruited to the viral genome to reverse this repression.

The present invention is related to a recombinant viral vector for vaccines.

Currently available poxvirus vectors for humans and other animals exhibit suboptimal expression of recombinant gene(s) and high expression of vector proteins which causes weak immunogenicity and high anti-vector immune response.

Herpes simplex viral infections, including herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2), are exceptionally common worldwide. These viruses establish lifelong persistent infections with cycles of lytic reactivation to produce recurrent diseases including oral and genital lesions, herpetic keratitis/blindness, congenital-developmental syndromes, and viral encephalitis. Infection with HSV-2 increases the rate of human immunodeficiency virus (HIV) transmission in coinfected individuals. DNA replication inhibitors are typically used to treat herpesvirus infections.

Shuttle vector for construction of recombinant MVA viruses.

Mutation in gene A34R can regulate the release of progeny virions from the surface of parental cells.