Given available therapies, drug resistance mutations will develop over time when selective pressure is exerted. Of greater concern is the likelihood that antiretroviral resistant HIV will disseminate in populations of HIV-infected people. There is urgent need for strategies to augment or extend the antiviral activity of antiretrovirals, and to allow for more effective treatment of HIV infection in heavily drug-experienced patients. Due to the selectivity of MA for the cellular targets of HIV infection and the potency of ABC, we tested this combination in primary peripheral blood mononuclear cells in vitro and found it profoundly synergistic in the inhibition of HIV, including HIV encoding multidrug resistance mutations. We arre performing a pilot clinical trial in patients with advanced AIDS and multidrug resistant HIV to test MA as a part of a salvage regimen.
Preliminary results suggest a profound antiviral and immunological response.
In parallel, detailed laboratory study of modulators of cellular metabolism in antiretroviral therapy may allow us to appreciate novel antiviral mechanisms of action, and lead to novel antiviral strategies. NRTIs Study the interaction of lymphocyte-selective inhibitors of pyrimidine metabolism and NRTIs. Severe hepatitis in three AIDS patients treated with the protease inhibitor indinavir. Abacavir and mycophenolic acid, an inhibitor of inosine monophosphate dehydrogenase, have profound and synergistic anti-HIV activity. J Acquir Immune Defic Syndr.