Chimeric protein constructs including a herpesvirus glycoprotein D (gD) and a heterologous polypeptide that interact with herpes virus entry mediator (HVEM) and enhance and enhance an immune response against the heterologous polypeptide and methods for their use are provided.

The present invention relates to methods and compositions for the prevention and treatment of herpes virus infections. The invention provides antigenic peptides, and pharmaceutical compositions comprising complexes of antigenic peptides and adjuvants that can activate an immune response against herpes viruses. The invention also provides methods of making the antigenic peptides and complexes of antigenic peptides and adjuvants. Methods of use of the pharmaceutical compositions are also provided.

The present invention relates to a live recombinant adenovirus vaccine and a combination therapy using the same for preventing infection of coronavirus infectious disease-19 (COVID-19), which occurred in Wuhan, China in 2019, and a rapid and harmless COVID-19 vaccine can be developed by producing an antibody specific to the novel coronavirus antigen using the recombinant adenovirus according to the present invention. In addition, through the combination therapy of the recombinant adenovirus vaccine and the compound according to the present invention, it is possible to more effectively and safely prevent or treat viral diseases such as COVID-19 as well as herpes simplex virus (HSV) infection.

The present invention provides vaccines for treating or preventing a herpes simplex virus infection and methods of using and making the vaccine. Further provided are recombinant herpes simplex virus genomes, recombinant viruses, and immunogenic compositions.

Modified and improved oncolytic viruses (and methods of use thereof) are disclosed. More particularly, modified and oncolytic human herpesviruses (and methods of use thereof) are disclosed, which include a modified amino acid sequence that includes a deletion in a region that represents the amino terminus of glycoprotein K. The modified and oncolytic human herpesviruses include a deletion of amino acid residues 31-68, relative to the wild type amino acid sequence of glycoprotein K in human herpesviruses. Isolated vector constructs that encode such oncolytic viruses are also disclosed. In addition, methods for using such oncolytic viruses to treat cancers are disclosed.

Chimeric protein constructs including a herpesvirus glycoprotein D (gD) and a heterologous polypeptide that interact with herpes virus entry mediator (HVEM) and enhance and enhance an immune response against the heterologous polypeptide and methods for their use are provided.

Provided herein are non-naturally occurring variants of the hepatitis B virus (HBV) Core protein, the HBV polymerase N-terminal domain, and the HBV polymerase C-terminal domain, as well as immunogenic fragments thereof. Fusion proteins comprising the HBV variants fused to a herpes simplex virus (HSV) glycoprotein (gD) sequence, as well as methods of using the fusion proteins, are also provided.

The present invention provides compositions for the prevention and treatment of genital herpes, comprising nucleoside modified mRNAs that encode herpes simplex virus (HSV) glycoproteins, including those involved in virus entry and immune evasion, and methods of use thereof.

It is an object of the present invention to develop a virus preparation comprising an oncolytic HSV having, in vivo, more effective cancer cell-killing activity than the antitumor effects of existing oncolytic HSVs. Specifically, the present invention relates to a virus preparation for the treatment of a cancer, comprising an HSV (herpes simplex virus) having a receptor-retargeted gD mutation and at least one membrane fusion activity-promoting region on the genome, and a method for treating cancer using the aforementioned virus preparation.

Methods of vaccinating, immunizing and/or treating a subject against a herpes simplex virus infection or a disease caused by a herpes simplex virus infection comprise administering to the subject an effective amount of a HSV-2 single-cycle virus and an effective amount of a recombinant HSV-2 glycoprotein D, wherein the HSV-2 single-cycle virus comprises HSV-2 having a deletion of glycoprotein D-encoding gene in the genome and the HSV-2 is phenotypically complemented with an HSV-1 glycoprotein D on a lipid bilayer of the HSV-2.