The present invention relates to a recombinant herpes simplex virus (HSV) containing an expression cassette capable of expressing a fused protein of a cancer-cell-targeting domain and an extracellular domain of HVEM and the use thereof. When the recombinant HSV infects and enters target cells, which are cancer cells, HSV proliferates, and an adapter, which is the fused protein, is expressed in the cells and is released to the outside of the cells along with the proliferated HSV virion upon cell lysis, or is released even before the virion is released due to cell lysis when the adapter contains a leader sequence, and the fused protein released to the outside of the cells acts to induce the HSV virion to infect surrounding cancer cells expressing a target molecule recognized by the cancer-cell-targeting domain or to increase the infection efficiency thereof.

The presently-disclosed subject matter relates to crosslinkers, compositions, and methods for trapping a target of interest on a substrate of interest. The methods may be used to inhibit and treat pathogen infection and provide contraception. The methods may be used to trap or separate particles and other substances. The subject matter further relates to methods of identifying and preparing optimal crosslinkers and methods for manipulating targets of interest.

The presently-disclosed subject matter relates to antibodies, compositions, and methods for inhibiting and treating virus infection in the respiratory tract and virus transmission through the respiratory tract. In particular, the presently-disclosed subject matter relates to inhibiting and treating virus infection in a subject using compositions and antibodies that trap viruses in mucus of the respiratory tract, thereby inhibiting transport of virus across or through mucus secretions.

Disclosed are compositions and methods for targeted treatment of CD99-expressing cancers. In particular, chimeric antigen receptor (CAR) polypeptides are disclosed that can be used with adoptive cell transfer to target and kill CD99-expressing cancers. Also disclosed are immune effector cells, such as T cells or Natural Killer (NK) cells, that are engineered to express these CARs. Therefore, also disclosed are methods of providing an anti-tumor immunity in a subject with a CD99-expressing cancer that involves adoptive transfer of the disclosed immune effector cells engineered to express the disclosed CARs. Also disclosed are multivalent antibodies are disclosed that are able to engage T-cells to destroy CD99-expressing malignant cells.

CRISPR/CAS-related systems, compositions and methods for editing HSV-1 genes in human cells are described, as are cells and compositions including cells edited according to the same. Methods for treating HSV-related keratitis using the said CRISPR/CAS-related systems, compositions and methods are also described.

Recombinant herpes simplex virus 2 (HSV-2) vaccine vectors, virions thereof, compositions and vaccines comprising such, and methods of use thereof are each provided.

A first aspect of the disclosure relates to the field of binding molecules targeted at pathogens. The disclosure further relates to proteinaceous binding molecules targeting cells displaying pathogen-associated molecular patterns, in particular targeting cell surface molecules associated with or derived from pathogens, more in particular cell surface proteins displaying peptides from intracellular (pathogen associated) proteins.

An engineered immune cell comprising a first functional exogenous receptor capable of binding and depleting natural killer (NK) cells, and a second functional exogenous receptor, wherein the engineered immune cell has reduced MHC I on cell surface.

An anti-HSV monoclonal antibody or an antigen-binding fragment thereof is an anti-HSV gB monoclonal antibody or an antigen-binding fragment thereof that specifically binds to herpes simplex virus (HSV) envelope glycoprotein B (gB), comprising: a heavy chain variable region comprising a heavy chain CDR1 consisting of the amino acid sequence set forth in SEQ ID NO: 3, a heavy chain CDR2 consisting of the amino acid sequence set forth in SEQ ID NO: 4, and a heavy chain CDR3 consisting of the amino acid sequence set forth in SEQ ID NO: 5; and a light chain variable region comprising a light chain CDR1 consisting of the amino acid sequence set forth in SEQ ID NO: 6, a light chain CDR2 consisting of the amino acid sequence set forth in SEQ ID NO: 7, and a light chain CDR3 consisting of the amino acid sequence set forth in SEQ ID NO: 8.

Disclosed herein are methods, reagents, and pharmaceutical compositions for modulating immune effector cell activation that does not require an antigen-specific antibody. The IgG Fc region is shown herein to contain both a domain that binds an FcR on immune effector cells and a non-overlapping region or domain that can bind Fc binding proteins on target cells, and that it is capable of bridging immune effector cells and target cells expressing Fc binding proteins without use of the antigen-binding region (Fab) of the antibody. Therefore, also disclosed are methods of enhancing or inhibiting passive ADCC in subjects.