| Human immunodeficiency virus is the foremost cause of acquired immunodeficiency syndrome. The current treatments do not focus on how in latent cells, the virus could still mutate. A drug resistant virus within the host will eventually lead to AIDS. Researchers must gain an appreciation of how latent cells function to keep the virus alive and away from immune response. In recent findings, the ability of HIV-1 to create its own viral microRNA from the TAR hairpin element is important for manipulating host cell mechanisms and maintaining latency. HIV-1 manipulates host cell mechanisms, such as cyclin dependent kinases and their corresponding cyclin elements, to suppress apoptotic cellular pathways and to maintain a latent infection. The therapeutic focus now turns to developing effective cdk inhibitors that eliminate viral replication, but do not affect normal cellular mechanisms. To do this, researchers need to understand the importance of how RNAi plays a role in viral activation and drug efficacy. A thorough understanding of HIV-1 microRNA pathways and latency could lead to alternative treatment options for HIV-1 infection. |
