Scientists discover bacterial toxin that can kill 'hidden' HIV

Washington: A genetically modified bacterial toxin can kill HIV-infected cells that persist despite treatment, an approach that could potentially be part of cure for the deadly virus, scientists say. The toxin, known as 3B3-PE38, targets HIV-infected cells and becomes internalised by them, shutting down protein synthesis and triggering cell death. A team including University of North Carolina and National Institutes of Health (NIH) scientists has demonstrated in a mouse model that the HIV-specific poison can kill cells in which the virus is actively reproducing despite antiretroviral therapy. [caption id=“attachment_1209151” align=“alignright” width=“380”]  Representational image: AFP[/caption] According to the researchers, such a targeted poison could complement antiretroviral therapy, which dramatically reduces the replication of HIV in infected cells but does not eliminate them. The 40 mice in the experiment were bio-engineered to have a human immune system. They were infected with HIV for several months and then given a combination of antiretroviral drugs for four weeks. Half of the animals subsequently received a two-week dose of a genetically designed, HIV-specific poison, or immunotoxin, to complement the antiretrovirals, while the other half continued receiving antiretrovirals alone. The scientists found that, compared to antiretrovirals alone, the addition of the immunotoxin significantly reduced both the number of HIV-infected cells producing the virus in multiple organs and the level of HIV in the blood. These findings, and results from previous studies, suggest that treating certain HIV-infected people with a combination of antiretrovirals and an immunotoxin might help achieve sustained disease remission, in which HIV can be controlled or eliminated without a lifetime of antiretroviral therapy, researchers said. The immunotoxin was created in 1998 in the laboratories of Edward A Berger of the National Institute of Allergy and Infectious Diseases, and Ira Pastan, of the National Cancer Institute. PTI