About the Technology

VIRTTU has taken the cold sore virus (Herpes simplex 1, HSV1), which affects 80% of the normal population, and modified it so that it cannot divide in normal cells in the body. However, the mutation we have engineered in the virus allows it to divide and multiply in cancer cells - thereby destroying the cancer cell. Our adapted virus SEPREHVIR®(HSV1716) is one of an exciting new class of cancer-destroying viruses (oncolytic viruses) that are now in development. The virus is unique in that it only divides in cancer cells and therefore kills only the malignant target without destroying normal tissue. The benefits for the patient from such a direct approach are enormous, with greatly reduced toxicity and side effects. 

Key Facts
  • Herpes simplex virus type-1 (HSV-1) is a common human virus that naturally infects most of the population.
  • HSV-1 normally causes few problems apart from cold sores.
  • Our product HSV1716 is a modified version of HSV-1 that is unable to replicate in tissues that normally support HSV-1 growth such as skin or brain.
  • HSV1716 lacks a single gene encoding a protein (ICP34.5) which is essential for virus replication and virulence in normal cells and tissues 
  • The lack of ICP34.5, makes HSV1716 non-virulent.
  • Cellular pathways exclusively active in cancer cells compensate for the loss of ICP34.5 resulting in specific oncolysis of the tumour cells, leaving normal cells intact.
  • HSV1716 is susceptible to approved antiviral drugs, such as acyclovir and gancyclovir, which potentially could be used to provide an additional safety net if ever required.

Mechanism of Action

Oncolytic viruses preferentially replicate in cancer cells. This occurs as cancer cells have specific pathways and proteins that are uniquely expressed and activated, making these cells susceptible to HSV1716 infection.

In normal cells, HSV1716 may be able to enter the cell but there are many powerful anti-viral mechanisms that prevent replication of our attenuated virus. In tumour cells, HSV1716 - with its deletion of ICP34.5 - can replicate as the tumour cell provides multiple ways to compensate for the absence of ICP34.5; so permitting viral replication and oncolysis.  Often these activated proteins and pathways are essential for the growth and survival of the cancer cells.

So the very mechanisms that promote tumour formation render it susceptible to destruction by SEPREHVIR®(HSV1716).

Please contact the team for our complete publications list.