[Human immunodeficiency virus and AIDS in terms of reverse transcriptase and molecular evolution].
Human immunodeficiency virus type 1 (HIV-1) evolves rapidly in the host. The computer analysis of the HIV-1 genome has shown that the mutation manner is dependent on oligonucleotide sequences (in particular, six bases long); thus HIV-1 adaptively evolves. The six-base-long interaction between template-primer oligonucleotide and the reverse transcriptase (RT) has been revealed by the crystal structure of RT, in vitro termination assay of plymerization, and hydroxyl radical footprint analysis. It has been thought that AIDS is caused by the large numbers of HIV-1 quasispecies yielded by the adaptive and rapid evolution in the host. However, the slow evolution and the high levels of viral RNA in the progressive HIV-1 infected individuals (progressives) were recently reported; in contrast, the adaptive and rapid evolution and the low viral-RNA levels were reported in the non-progressives. This suggests that the physiological environment, e.g. pH and dNTP balance, in which RT works in the progressives is different from that in the non-progressives.
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Fujitsu Laboratories Ltd., ERATO, Japan Science and Technology Corporation (JST).
D000163:Acquired Immunodeficiency Syndrome / Q000821:virology*; D001483:Base Sequence; D018450:Disease Progression; D004352:Drug Resistance, Microbial / Q000235:genetics; D019143:Evolution, Molecular; D015752:Genes, env; D016679:Genome, Viral; D054303:HIV Reverse Transcriptase; D015497:HIV-1 / Q000201:enzymology / Q000235:genetics; D006801:Humans; D009154:Mutation; D009841:Oligonucleotides
D009841:Oligonucleotides; D054303:HIV Reverse Transcriptase