Researchers at Ben-Gurion University of the Negev (BGU) have made a significant breakthrough, discovering similarities between Leukemia and HIV that might hold the key to developing a clinical solution to prevent and destroy the virus.
“Similar to what happens with the HIV virus when it enters a chronic state, reproduction mechanisms control the expression of the genes responsible for hematopoietic STEM cells – the first cells that develop, ” says Dr. Ran Taube, of BGU’s Shraga Segal Department of Microbiology and Immunology.
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“This research is based on the assumption that damage to the mechanisms of expression and reproduction of the viral genome is responsible for the accumulation of the latent HIV virus and leads to the chronic disease condition.”
Dr. Taube’s team, in collaboration with Dr. Uri Rubio of Soroka University Medical Center, is seeking innovative ways to “wake up” the virus from its silent active state, while at the same time applying anti-retrovirals to essentially eradicate the virus completely.
“Until now, the medical community researchers had very limited information on the existence of a connection between AIDS, caused by the HIV virus, and a rare blood cancer, known as Mixed Lineage Leukemia (MLL), ” explains Dr. Taube. “MLL, found mostly in children, hinders blood system cell development.” Dr. Taube’s research detects mechanisms of action that are similar to the development of the blood cancer MLL.
Although, in recent years, AIDS has been effectively treated with anti-retroviral medications, these do not prevent infections, so their efficacy is limited. Also, there are a small number of inactive, latent viral particles found in the body that are not affected by the anti-retroviral drugs. These viruses are hidden in the body, can effectively avoid the immune response, and at any moment can multiply and infect new cells.
There is still no vaccine and no treatment has been found to prevent the spread of the HIV virus and the number of people who are infected with the virus continues to rise each year.