Abstract: Disclosed herein are recombinant CMV vectors which may comprise a heterologous antigen that can repeatedly infect an organism while inducing a CD8+ T cell response to immunodominant epitopes of the heterologous antigen. The CMV vector may comprise a deleterious mutation in the US11 glycoprotein or a homolog thereof.

Abstract: Disclosed herein are recombinant CMV vectors which may comprise a heterologous antigen that can repeatedly infect an organism while inducing a CD8+ T cell response to immunodominant epitopes of the heterologous antigen. The CMV vector may comprise a deleterious mutation in the US11 glycoprotein or a homolog thereof.

Abstract: Disclosed herein are recombinant CMV vectors which may comprise a heterologous antigen that can repeatedly infect an organism while inducing a CD8+ T cell response to immunodominant epitopes of the heterologous antigen. The CMV vector may comprise a deleterious mutation in the US11 glycoprotein or a homolog thereof.

Abstract: Disclosed herein are recombinant CMV vectors which may comprise a heterologous antigen that can repeatedly infect an organism while inducing a CD8+ T cell response to immunodominant epitopes of the heterologous antigen. The CMV vector may comprise a deleterious mutation in the US11 glycoprotein or a homolog thereof.

Abstract: Disclosed herein are recombinant CMV vectors which may comprise a heterologous antigen that can repeatedly infect an organism while inducing a CD8+ T cell response to immunodominant epitopes of the heterologous antigen. The CMV vector may comprise a deleterious mutation in the US11 glycoprotein or a homolog thereof.

Abstract: Disclosed herein are recombinant CMV vectors which may comprise a heterologous antigen that can repeatedly infect an organism while inducing a CD8+ T cell response to immunodominant epitopes of the heterologous antigen. The CMV vector may comprise a deleterious mutation in the US 11 glycoprotein or a homolog thereof.

Abstract: Applicants have used microarrays, gene expression profiling, and gene silencing methods to identify and provide a plurality of ‘validated’ virus-induced cellular gene sequences (e.g., HMG20B, HRH1, NP and c-YES (src family kinases)) and pathways useful as therapeutic targets for modulation of viral-mediated cellular effects. Particular embodiments provide therapeutic compositions, and methods for modulation of viral infection, replication, maturation, progression, or other virally-related conditions or diseases, comprising inhibition of virally-induced gene sequences and gene products. Additional embodiments provide screening assays for compounds useful to modulate viral infection, replication, maturation or progression, or viral-related conditions or diseases. Further embodiments provide diagnostic and/or prognostic assays for viral infection, replication, maturation or progression. Preferably, the viruses all selected from the group consisting of retroviruses (e.g.

Abstract: The present invention uses gene expression profiling, and gene silencing methods to identify and provide a plurality of ‘validated’ KSHV-induced cellular gene sequences and pathways useful as targets for modulation of KSHV-mediated effects on cellular proliferation and phenotype (e.g., cancer) associated with latent and lytic phases of the Kaposi's sarcoma-associated herpesvirus (KSHV; Human herpesvirus 8; HHV8) life cycle. Particular embodiments provide therapeutic compositions, and methods for modulation of KSHV infection or KSHV-mediated effects on cellular proliferation and phenotype, comprising inhibition of KSHV-induced gene sequences. Additional embodiments provide screening assays for compounds useful to modulate KSHV infection or KSHV-mediated effects on cellular proliferation and phenotype. Further embodiments provide diagnostic and/or prognostic assays for KSHV infection.

Abstract: According to the present invention, eight human RING-CH-containing genes are human transmembrane ubiquitin ligase proteins, are homologues of the viral K3-family, and perform functions similar to their viral counterparts. One of these proteins, MARCH-IV, is able to downregulate MHC I and CD4 in a fashion similar to that afforded by the viral immune evasion proteins. This is the first cellular gene product identified that downregulates surface expression of MHC I. The MARCH-family of proteins regulates endocytosis of cell surface receptors (e.g., transferrin receptor, histocompatibility antigens and Fas; type I as well as type II transmembrane domains) via ubiquitination. Particular embodiments provide drug targets for inhibiting the internalization and degredation of various cell surface receptors. Further embodiments provide methods for treating or preventing cancer and other disorders (e.g.