Summary On Retargeting Of Herpes Simplex Virus

“Retargeting of Herpes Simplex Virus (HSV) vector”, published by Virology in 2016, written by Goins F. W et al. Here the topic mention is on Herpes Simplex Virus (HSV), a genital infection that affects human skin and the nervous system. This article come with a main purposes that was based on how HSV is been retargeted. Retargeting was achieved in one way where HSV encodes 12 glycoproteins which come from the different viruses with different hostage range. Another way for HSV to be retargeted was to amend any of the previous glycoproteins that are present or any proteins that are coat and are combined to peptide ligands or a single chain antibodies (scFvs) that are bound to a specific receptor. When the envelopes of glycoproteins are connected to the unlimited amount of cellular receptors for HSV they are altered for vaporising natural receptor binding and absorb ligands, or (scFv) which recognises the human epidermal growth factor (EGF) receptor 2 (HER2).

This becomes a challenge for retargeting HSV when 12 glycoproteins entering they are contributed to viral tropism because each enveloped virus will use some glycoproteins in order to bind and enter the targeted cells. Examples of these viruses are measles, influenza or HIV, which can employable achieve cell binding and entry, but also being dependent on glycoproteins which can enter an infect cell and spread out to make the cells unaffected of HSV.  Alternatively, HSV is retargeting by having soluble adapters that can recognise virus and the specific receptor in a targeted cell when engaged to HSV. To achieve a full retargeting, HSV it is required for the virus to have a connection with the canonical HSV entry receptors that must be blocked/ removed and functionally substituted with an alternate ligand-receptor interaction.  When the choice of alternate receptors is limited to candidates that are indicators for the target cells and are familiar by peptide ligands (scFvs). which preferentially are not activated to a standard biological function of the receptor.

By retargeting HSV, it has a purpose of engineering oncolytic HSVs (oHSV), a process that replicates tumor cells and cause destruction to the formation of progeny virions which can spread to adjacent tumour cells. Another article suggests that to completely retarget HSV vectors up to date are replication-competent of oHSVs’. By replication-competent virus are infected to kill cancer cells as an innovative strategy against tumours such as a brain tumour, breast and ovarian cancer. It suggests that HSV can be used as a drug to control unwanted viruses and can retarget viruses in an expression of the receptor of choice in the targeted tumour. For example, HER2 appears to be a good target against brain tumours because it is absent in normal adult central nervous system. Furthermore, another article suggests that HER2, as a member of EGFR, occurs not just in breast and ovary cancers,  but also in stomach, lungs and other cancers. Here retargeting can be achieved when engineering gD (scFv) to HER2, derived from a cancer drug known as trastuzumab, and by appropriate deletions in gD, which remove critical residues for interaction with HVEM, which stands for herpesvirus entry mediator.