To increase the therapeutic potential of these oncolytic viruses based on a 24 base pair deletion in the viral E1 A gene (D24), a conditionally replicating adenovirus targeting multiple receptors upregulated on tumors was generated by incorporating an Ad5/3 fiber with a carboxyl terminus RGD ligand. The virus displayed full cytopathic effect in tumor lines assayed at low titers with improved cytotoxicity over Ad5-RGD D24, Ad5/3 D24 and an HSV oncolytic virus. The virus was further engineered to deliver immunotherapeutic agents such as GMCSF while maintaining enhanced heterogenic oncolysis.

Provided herein are recombinant viruses and artificially coated delivery systems, and methods of use.

Disclosed are recombinant adenoviral compositions and methods for their use in treating disorders associated with epithelial tissues.

The present invention relates to a novel adenoviral vector not including a replication competent adenovirus. A recombinant E1/E3/E4-deleted adenoviral vector, of the present invention, in which an antigenic protein and an E4orf6 gene are inserted in an E1 gene-deleted region, has adenovirus productivity, degree of antigen expression, neutralizing antibody production amount, and T cell induction ability that are similar to those of a control group, and thus can be effectively used as a carrier for various vaccines for diseases or anti-cancer vaccines.

The present disclosure includes adenoviral vectors characterized by efficient transduction of HSCs, e.g., for in vivo gene therapy. The present disclosure includes, among other things, Ad3, Ad7, Ad11, Ad14, Adpatentdocket@choate.com16, Ad21, Ad34, Ad37, and Ad50 vectors and genomes. Ad3, Ad7, Ad11, Ad14, Ad16, Ad21, Ad34, Ad37, and Ad50 vectors and genomes of the present disclosure can include therapeutic payloads.

Producing adenovirus gene therapy vector in producer cells that express or over-express adenoviral polypeptide IX enables one to produce pIX-deleted adenovirus in suspension cell culture. Using producer cells that express or over-express adenoviral polypeptide IX also increases the yield of adenovirus vector, regardless of whether that adenovirus is pIX-deleted. Using producer cells that express or over-express adenoviral polypeptide IX also improves the resulting vector's transduction kinetics, reducing the number of pfu/target cell required to achieve a given level of transduction/infection, shortening the time the vector requires to transduce or infect a target cell, and shortening the time an infected target cell produces progeny virus.

Provided are chimeric oncolytic adenoviruses simultaneously expressing IL-12, IFN-?, and CCL5, and an application thereof in tumor treatment. A capsid protein hexon of the oncolytic adenovirus is formed from chimerizing hexon sequences of the two serotype viruses Ad5 and Ad48, and a fiber protein is formed from chimerizing fiber sequences of the two serotype viruses Ad5 and Ad11. The chimeric oncolytic adenovirus can activate intrinsic anti-cancer activity of a variety of viral structural proteins, the ability to infect tumor cells is increased while also ensuring that the virus itself avoids interception from pre-existing neutralizing antibodies and adhesion and uptake of hepatocytes, and an effect of killing cancer cells is enhanced.

The present invention relates to novel vaccines against Human papillomavirus (HPV) infections, based on recombinant capsid-display adenovirus vectors. Described are capsid modified replication deficient adenovirus particles encoding and displaying multiple HPV L2 antigenic fragments, via a minor capsid protein IX, and their use for eliciting an immune response in order to provide protection against infections from multiple HPV types.

The invention relates to an adenovirus comprising a nucleic acid sequence encoding a Helicobacter pylori neutrophil-activating protein (NAP) and/or a nucleic acid sequence encoding an immunologically equivalent fragment of NAP and a nucleic acid sequence encoding an immunomodulator capable of inducing an immune response in a subject. The adenovirus has enhanced clinical effects in terms of delaying tumor growth and prolonging survival.

Modified E1a regulatory sequences are provided, wherein at least one Pea3 binding site, or a functional portion thereof, is deleted. Also provided are modified E1a sequences that selectively express particular isoforms. Also provided is an E1b-19K clone insertion site. These modified sequences can be used individually, or in combination with one another, to provide tumor-selective expression of proteins.