HIV-1 Exploits Cellular miR-2909 RNomics to Initiate and Ensure AIDS Disease

Human immune cells have evolved with a membrane trafficking pathway called Autophagy, responsible for engulfing the invading pathogens and thereby equipping these cells with the innate and adaptive immune responses against numerous pathogens. On the other hand, the various pathogens have developed strategies to either block or use the autophagy mechanism to their own advantage [1]. Human immunodeficiency virus type 1 (HIV-1) infects mainly CD4+ Tlymphocytes and macrophages through the interaction of the viral (Env) glycoproteins (Gp120 and Gp41) with CD4 as well as coreceptor, mainly CCR5, expressed at the surface of the target cells. Such type of interaction induces a structural rearrangement in glycoprotein 41 and the insertion of its N-terminus fusion peptide into the target cell membrane, leading to the cellular endocytosis of the HIV-1 viral particles [2]. The HIV-1 replication cycle is governed in two phases: the early phase, from viral entry to provirus integration with cellular genome, and the late phase, from transcription of viral genes to the release of new particles [2].