Transduction to tumour cells by retargeting is important for

targeting can be used to limit viral vector infection to targeted cells 1. Those vectors
either magnify the tropism of viruses that infect a very limited number of cell
types or limit the tropism of viruses that infect many cells of the host. In
the article Retargeting of herpes
simplex virus (HSV) vectors 1, four different strategies are explored to design
retargeting HSV vectors. Glycoprotein from other viruses can be inserted in
place of HSV glycoproteins. The G glycoprotein from vesicular stomatitis virus
(VSV-G) can be used to pseudotype various viruses. Peptide ligands for
naturally occurring receptors can be introduced into either HSV gD or gC.
Peptide ligands can replace receptor binding introduced into the HSV gD and gH
genes. Sequences encoding single chain antibodies (scFvs) can be introduced
into the HSV gD and gH genes. In order to attain entry via specific target
receptor, HSV can also be mixed with soluble adapter before infection; soluble
adapter molecules are capable of binding to HSV gD and to the cell surface
receptor target.


area of research is exceptionally relevant to gene therapy to develop
alternative to drugs and radiation therapies 1,2, e.g. in the treatment of chronic pains,
solid tumours, hematologic malignancies etc.
Efficient delivery of
oncolytic HSV-1 to tumour cells by retargeting is important for patients whose
immune system is compromised. HSV-1 has been thoroughly studied in
oncolytic viral therapy 2. Researches on the different
systems to enhance HSV-1 delivery into cells have emerged (e.g. chemical
sensitizers, anti-tumour enhancing, chelation etc.). Novel information on individual amino
acids and functional domains of gD, gC, gB and gH/gL has enable the use of HSV
retargeting 1,3,4.
Furthermore, studies on HSV ability to co-exist with their host cells have aided
the design of HSV retargeting as well as oncolytic viral therapy 1,2,3. HSV
infection can be reduced by host immune system response; howbeit latently
infected cells may persist while the viruses maintain a fine-tuned and delicate
balance with the host 3.

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successful studies have been performed to limit oHSV infection to only specific
tumour cell type, more research is needed to help understand the numerous factors
(viral factors and cellular host factors) influencing herpes viruses infection 2. It is
still unclear how redundancy or/and latency might be key to HSV strategy to
infect different cell types in various tissues 1,2,5. oHSV-1 therapy remain relatively
safe, since unlike other adenoviruses, it does not integrate into the host
genome 2. Redundancy can overtake
host defences but stages of differentiation or maturation of a cell may enable
or inhibit HSV integration 3. The task of retargeting HSV is complex due to the various
HSV glycoproteins involved in the process of attachment and entry. Nevertheless,
although depictions and language
currently used are inadequate to productively consolidate new data into the
present hypothesises 5, the
introduction of peptide ligands as a retargeting approach has been conclusive 1.


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