The latest worldwide HIV/AIDS news and updates, including treatment, prevention, and hepatitis and TB co-infections.Two studies published last month described promising new approaches which could stop HIV infecting cells. They could either eliminate or permanently suppress the activity of the so-called ‘reservoir’ cells which are the source of new virus in people taken off antiretroviral therapy (ART), and are the reason HIV infection is lifelong.The first class of drugs starve cells of the 'fuel' they need to produce HIV, while the second permamently suppresses the spark that ignites that fuel, so to speak.A team from the Institut Pasteur in Paris found that the vulnerability of T-cells to infection was critically dependent on how fast they are metabolising – how high their energy demand is and how fast they are turning fuels like glucose into energy. It found that cells with a high energy consumption are far more vulnerable to infection, and that although their speed of metabolism did correlate to what kind of T-cell they were, it was an independent kind of vulnerability to HIV that could be targeted by a new class of drugs. By slowing down cells’ metabolism by feeding them with a ‘dummy’ inactive form of glucose called 2-DG, they were able to selectively kill HIV-infected cells in the lab dish, even ones not actively producing HIV. One advantage of 2-DG is that it can be produced cheaply and is already under investigation in cancer, as a way of ‘starving’ tumour cells of energy. In the other study a team from the University of Pittsburgh screened a number of compounds that interfere with the genetic process that cause cells to become active – which means, in the case of HIV reservoir cells, that they start producing virus again. If cell activation, even off ART, could be prevented, then this would provide long-term remission from HIV infection – a so-called functional cure.This potential cure strategy has been called ‘block and lock’ by researchers, as it depends on suppressing HIV reservoir cells, as opposed to ‘kick and kill’, which is based on activating them. The first compound capable of doing this, called dCA, was found in experiments on mice in 2015. The Pittsburgh team screened a number of other compounds for similar activity and found one, PF-3758309, which was active at very low doses. The next part of the research will look at whether its suppressive effects in reservoir cells persist. PF-3758309 is also under investigation as a cancer therapy.
HIV & AIDS Information :: Two new types of cell therapy could target reservoir cells and permanently stop HIV infection