Genes common to both the human T-cell leukemia virus and high-risk human papillomaviruses activate survival mechanisms in cancer cells. An SMU lab, with National Cancer Institute funding, is hunting ways to inhibit those genes to halt the development of cancer.
In 1996 the introduction of "triple cocktail" drug therapy transformed AIDS from a death sentence into a manageable chronic disease. The drug regimen, also known as HAART for highly active antiretroviral treatment, involved treating patients with three or more classes of antiviral medicines.
But the virus fought back. It mutates easily, and the mutations caused resistance to first one and then another drug making up the cocktail. Unsettling reports of newly infected patients with the drug-resistant virus meant researchers needed to find new ways to fight HIV infection.
In his third-floor laboratory in Dedman Life Sciences Building, biologist Robert Harrod and his team are zeroing in on a new way to inhibit the virus that causes AIDS. They already have shown that their approach, which involves the rare genetic disorder Werner syndrome, works when the disorder's enzyme defect is introduced into cells.
Now they are trying to find practical ways to use this pathway to inhibit the AIDS virus. The beauty of this approach is that the AIDS virus will not be able to mutate in a way that can defeat this treatment, says Harrod, associate professor in the Biological Sciences Department of Dedman College.