Disclosed herein, in certain embodiments, are recombinant myxoma viruses (MYXVs) and nucleic acid constructs encoding the recombinant MYXVs. In some embodiments, the MYXVs are engineered to inactivate or attenuate an activity or expression level of an M153 protein. In some embodiments, the MYXVs are engineered to express one or more transgenes such as a tumor necrosis factor (TNF), interleukin-12 (IL-12), or decorin. Also disclosed herein, in certain embodiments, are methods of using the MYXVs. Some embodiments include providing a MYXV as described herein to a subject in need thereof.

Disclosed herein, in certain embodiments, are recombinant myxoma viruses (MYXVs) and nucleic acid constructs encoding the recombinant MYXVs. In some embodiments, the MYXVs are engineered to inactivate or attenuate an activity or expression level of an M153 protein. In some embodiments, the MYXVs are engineered to express one or more transgenes such as a tumor necrosis factor (TNF), interleukin-12 (IL-12), or decorin. Also disclosed herein, in certain embodiments, are methods of using the MYXVs. Some embodiments include providing a MYXV as described herein to a subject in need thereof.

There are provided antigens, vectors encoding the antigens, and antibodies and other binding compounds to the antigens and uses thereof in the prevention or treatment of malaria. In particular, compositions are provided comprising fragments of Reticulocyte-binding protein Homologue 5 (PfRH5). In particular, the invention provides fragments of PfRH5 rationally designed on the basis of the PfRH5 crystal structure, wherein said fragments which lack disordered regions, particularly the flexible N-terminal region and/or flexible central linker.

Disclosed herein, in certain embodiments, are recombinant myxoma viruses (MYXVs) and nucleic acid constructs encoding the recombinant MYXVs. In some embodiments, the MYXVs are engineered to inactivate or attenuate an activity or expression level of an M153 protein. In some embodiments, the MYXVs are engineered to express one or more transgenes such as a tumor necrosis factor (TNF), interleukin-12 (IL-12), or decorin. Also disclosed herein, in certain embodiments, are methods of using the MYXVs. Some embodiments include providing a MYXV as described herein to a subject in need thereof.

Disclosed herein, in certain embodiments, are recombinant myxoma viruses (MYXVs) and nucleic acid constructs encoding the recombinant MYXVs. In some embodiments, the MYXVs are engineered to inactivate or attenuate an activity or expression level of an M153 protein. In some embodiments, the MYXVs are engineered to express one or more transgenes such as a tumor necrosis factor (TNF), interleukin-12 (IL-12), or decorin. Also disclosed herein, in certain embodiments, are methods of using the MYXVs. Some embodiments include providing a MYXV as described herein to a subject in need thereof.

Compositions, methods, and kits are provided for treating CCR8 mediated diseases with applicability to atopic dermatitis and potential applicability to asthma, prurigo nodularis, nummular dermatitis, neurodermatitis, and lichen simplex chronicus and some lymphomas, multiple sclerosis, acquired immunodeficiency disease, peritoneal adhesions, Kaposi's sarcoma and atherogenesisthe expression of all of which, at least in part, is mediated by cells expressing the chemokine receptor CCR8. The compositions include proteins and fusion proteins from Molluscum contagiosum Virus (MCV) or variants, analogs and derivatives thereof which exhibit inhibitory activity. Examples of such MCV proteins are MC148 fusion protein (MC148fp) identified as MC148P-TAT-6xHis (6xHis disclosed as SEQ ID NO: 11), and its variants, fragments, analogs and derivatives which possess inhibitory activity. The variants, fragments, analogs and derivatives of MC148p and of MC148fp may be less than 100% homologous to MCV proteins as long as they are sufficiently homologous that inhibitory activity is preserved.

Disclosed here are polypeptides, derived from the Myxomavirus-derived secreted glycoprotein, M-T7, comprising point mutations that interfere with chemokine-glycosaminoglycan binding. Compositions containing such M-T7 derived polypeptides with point mutations are therefore useful in preventing, blocking and/or reducing rejection of a transplant.

Disclosed here are polypeptides, derived from the Myxomavirus-derived secreted glycoprotein, M-T7, comprising point mutations that interfere with chemokine-glycosaminoglycan binding. Compositions containing such M-T7 derived polypeptides with point mutations are therefore useful in preventing, blocking and/or reducing rejection of a transplant.

There are provided antigens, vectors encoding the antigens, and antibodies and other binding compounds to the antigens and uses thereof in the prevention or treatment of malaria. In particular, compositions are provided comprising fragments of Reticulocyte-binding protein Homologue 5 (PfRH5). In particular, the invention provides fragments of PfRH5 rationally designed on the basis of the PfRH5 crystal structure, wherein said fragments which lack disordered regions, particularly the flexible N-terminal region and/or flexible central linker.

In one aspect, composition generally includes a virotherapeutic agent and an inhibitor of tumor necrosis factor (TNF). In one or more embodiments, the virotherapeutic agent can include an oncolytic virus. In one or more embodiments, the inhibitor of TNF comprises can include an antibody, or a fragment thereof, that binds to TNF. In another aspect, a method of treating a tumor in a subject generally includes co-administering to the subject an oncolytic virotherapeutic agent and an inhibitor of tumor necrosis factor (TNF). In one or more embodiments, the oncolytic virotherapeutic agent is administered intratumorally. In one or more embodiments, the inhibitor of TNF is administered systemically.