As is known, human immunodeficiency virus (HIV) is the etiological agent of acquired immunodeficiency syndrome (AIDS), a devastating disorder of the human immune system, usually with fatal outcome [1]. The main targets for this retrovirus in the human organism are the CD-4 receptor bearing cells of the immune system. During HIV infection, the absolute number of T-cells with the CD-4+ cell phenotype sharply decreases both as a result of direct virus action and, indirectly, via apoptosis mechanisms. A common structural feature of the nucleoside analogs used for the therapy of HIV-infected patients is modification of the nucleoside at the 3 -position of the deoxyriboside ring [2]. The mechanism of the anti-HIV effect of these drugs is based on the conversion of nucleosides into their triphosphate forms under the action of cell kinases. These triphosphates may serve as the substrates for both the reverse transcriptase (RT) of the virus [3, 4] and the cell DNA polymerase, thus acting as chain growth terminators upon inclusion in the DNA sequence [5]. Various 3 -substituted nucleoside analogs exhibit different antiviral activity. However, a relationship between the structure and activity for these preparations is not explicit, which is probably related to the fact that the formation of triphosphates requires a stepwise activation process involving substrate recognition by several enzymes [4, 6]. In addition, some dideoxynucleosides are subject to restricted phosphorylation in the cell because of a certain structural difference from the natural nucleosides [3]. To the present, the main drug used for the therapy of AIDS patients is 3 -azido-3 -deoxythymidine (azidothymidine, AZT) [7]. In addition, the complex therapy employs two other dideoxynucleosides: 2 ,3 -dideoxyinosine [8] and 2 ,3 -dideoxycytidine [9]. The experience gained in using AZT (I) revealed significant drawbacks of this anti-HIV agent, such as the need to administer the drug in large doses and the drug’s effect upon DNA reparation in the CNS. As a result, prolonged administration of I leads to side effects such as impaired memory, violated motor function, and some other neuropathological manifestations [10]. However, the main disadvantage of I (as well as of the other nucleoside analogs) is related to the appearance of various HIV modifications resistant to this drug. This circumstance stimulates researchers to seek new active preparations with a mechanism different from that of I.