Using Viruses To Fight Dormant HIV Cells

Researchers from The Ottawa Hospital have discovered that the MG1 Maraba virus has the ability to both target and destroy the kind of HIV infected cells standard antiretroviral therapies are not currently able to. If it is found that this treatment works in human, it may possibly contribute to a cure for HIV. Laboratory findings have been published in the Journal of Infectious Diseases.

It is made possible to keep the level if HIV virus in the blood low with the use of a daily cocktail of medications. There is currently not a way to available in which to completely eliminate the dormant HIV infected cells from within the body. If a person living with HIV were to stop taking the antiretroviral medications the hidden viruses would make a rapid rebound.

It is difficult to target and identify infected cells because they are not distinguishable from those of normal healthy cells. A new approach to identifying these dormant cells was devised by Dr. Jonathan Angel and his team using the MG1 virus. The MG1 virus is known to attack cancer cells which have defects in their pathways, making the cells vulnerable to viruses. The team had found that the HIV infected cells also contain defects in their pathways.

Using a number of HIV infected laboratory animals researchers were able to observe that the MG1 virus did target and eliminate the infected cells while leaving the healthy cells unharmed.

According to Angel they thought the cells had similar characteristics, and they were right.

Most of these cells are in the lymph nodes and other organs, a small number are found in the blood. When MG1 was added to the relevant blood cells, the level of HIV DNA in the sample dropped, indicating that the HIV infected cells had been eliminated.

The next phase in this research is to try the virus in animal HIV models, or even possibly move directly to clinical trials.

Angel states they know the MG1 virus is targeting and killing the HIV infected cells, but it is not known exactly how, it may be because of the impaired interferon pathway, more research is needed to know for certain.