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lüll Antiviral therapy for human immunodeficiency virus infections De Clercq EClin Microbiol Rev 1995[Apr]; 8 (2): 200-39Depending on the stage of their intervention with the viral replicative cycle, human immunodeficiency virus inhibitors could be divided into the following groups: (i) adsorption inhibitors (i.e., CD4 constructs, polysulfates, polysulfonates, polycarboxylates, and polyoxometalates), (ii) fusion inhibitors (i.e., plant lectins, succinylated or aconitylated albumins, and betulinic acid derivatives), (iii) uncoating inhibitors (i.e., bicyclams), (iv) reverse transcription inhibitors acting either competitively with the substrate binding site (i.e., dideoxynucleoside analogs and acyclic nucleoside phosphonates) or allosterically with a nonsubstrate binding site (i.e., non-nucleoside reverse transcriptase inhibitors), (v) integration inhibitors, (vi) DNA replication inhibitors, (vii) transcription inhibitors (i.e., antisense oligodeoxynucleotides and Tat antagonists), (viii) translation inhibitors (i.e., antisense oligodeoxynucleotides and ribozymes), (ix) maturation inhibitors (i.e., protease inhibitors, myristoylation inhibitors, and glycosylation inhibitors), and finally, (x) budding (assembly/release) inhibitors. Current knowledge, including the therapeutic potential, of these various inhibitors is discussed. In view of their potential clinical the utility, the problem of virus-drug resistance and possible strategies to circumvent this problem are also addressed.|Antiviral Agents/chemistry/pharmacology/*therapeutic use[MESH]|Base Sequence[MESH]|Drug Resistance, Microbial[MESH]|Drug Therapy, Combination[MESH]|HIV Infections/*drug therapy/virology[MESH]|HIV Reverse Transcriptase[MESH]|HIV/drug effects/physiology[MESH]|Humans[MESH]|Molecular Sequence Data[MESH]|Reverse Transcriptase Inhibitors[MESH]|Virus Integration/drug effects[MESH]|Virus Replication/drug effects[MESH] |