Oncolytic viruses are known to stimulate the antitumor immune response by specifically replicating in tumor cells.
Among mammalian reoviruses, reovirus type 3 Dearing (T3D) specifically replicates in cancer cells, resulting in efficient tumor cell lysis but not in normal tissues.
(1, 2) This idea was exemplified by an adenoviral vector that specifically replicates in p53-deficient cells, a genetic feature often associated with cancer cells.
Oncolytic herpes simplex virus (HSV) vectors that specifically replicate in and kill tumor cells sparing normal cells are a promising cancer therapy.
Reoviruses are naturally occurring viruses that are non-pathogenic and have been reported to specifically replicate in cancer cells with an activated Ras pathway but not in normal tissue.
Other oncolytic viruses including reovirus, measles virus, VSV and NDV, seem to have an inherent capability to specifically replicate only in tumor cells, leaving normal cells largely unaffected.
Oncolytic herpes simplex virus-1 (HSV-1) is designed to specifically infect, replicate in, and lyse cancer cells.
The mutagenicities of (6 R,8 R)- and (6 S -crotonaldehydehyde adductS -crotonaldehyde1, row 18 adducts were ∼5 and ∼6%, respectively, when a single-stranded, site specifically modified vector was replicated in the COS-7 system (76).
More specifically, the techniques used can be replicated in future validation studies.
This matching approach could be replicated in other settings, specifically large datasets which contain some or all of the same individuals and which include common clinical and demographic variables but no unique identifiers, for example, investigating the transition from adolescent to adult HIV-care by matching these separate datasets.
