title: [Genotypic antiretroviral resistance testing and phylogenetic analysis of protease and reverse transcriptase in antiretroviral drug-naïve AIDS patients in Henan province].
abstract: OBJECTIVE
  Frequency, type and clinical implications on protease and reverse transcriptase drug resistance mutations were investigated and phylogenetic analysis in antiretroviral drug-naïve AIDS patients was carried out in Henan province.
  
  
  METHODS
  45 plasma samples were separated from the anticoagulatory whole blood, from which reverse transcription-polymerase chain reaction technique was used to amplify the partial pol gene. The sequences were analysed for genotypic antiretroviral resistance and phylogenetic relation through landing the websites http://hivdb.stanford.edu and http://hiv-web.lanl.gov, under BioEdit and DNAClub software.
  
  
  RESULTS
  Partial pol sequences of 36 samples were successfully amplified. The major mutation rate of resistance to protease was 8.3% (3/36), including types D30A, V32A, G73C and V82A. Minor mutation rate of resistance was 100%, including types of L63PS (36/36), I93L (35/36), V77IL (34/36), A71IVT (10/36) and D60E (2/36). The mutation rate of resistance to reverse transcriptase was 38.9% (14/36). Mutation-scoring and clinical implication clewed drug resistance rates were 5.6% (2/36) and 22.2% (8/36) to protease inhibitors and reverse transcriptase inhibitors respectively, while 1 sample was potentially low-level resistant to all of the protease inhibitors and 3 samples to part of the reverse transcriptase inhibitors. Phylogenetic analysis revealed that the pol gene of 36 samples were highly homologous and having a near relative to B.US.83.RF ACC M17451. 36 samples seemed to have the same infection source while their resistance mutations were not due to drug-resistant virus infection but to the evolving of virus in vivo.
  
  
  CONCLUSIONS
  Most of the antiretroviral drug-naïve AIDS patients in Henan province were sensitive to the currently available antiviral medicine, but antiviral treatment must be in accordance with the strict procedure and to keep better adherence, to avoid the epidemics caused by drug-resistant virus.
authors.affiliation: Insitute of Microbiology and Epidemiology, Beijing 100071, China.
authors.forename: Kun
authors.initials: K
authors.lastname: Yang
authors.forename: Jing-yun
authors.initials: JY
authors.lastname: Li
authors.forename: Zuo-yi
authors.initials: ZY
authors.lastname: Bao
authors.forename: Han-ping
authors.initials: HP
authors.lastname: Li
authors.forename: Lin
authors.initials: L
authors.lastname: Li
authors.forename: Dao-min
authors.initials: DM
authors.lastname: Zhuang
authors.forename: Zhe
authors.initials: Z
authors.lastname: Wang
authors.forename: Hong
authors.initials: H
authors.lastname: Li
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000235:genetics*; D000328:Adult; D019380:Anti-HIV Agents / Q000494:pharmacology*; D002681:China; D024882:Drug Resistance, Viral / Q000235:genetics*; D005260:Female; D015751:Genes, pol / Q000235:genetics; D005838:Genotype; D016333:HIV Protease / Q000235:genetics*; D017320:HIV Protease Inhibitors / Q000494:pharmacology; D006801:Humans; D008297:Male; D009154:Mutation; D010802:Phylogeny; D012194:RNA-Directed DNA Polymerase / Q000235:genetics*; D018894:Reverse Transcriptase Inhibitors / Q000494:pharmacology
chemical_list: D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors; D012194:RNA-Directed DNA Polymerase; D016333:HIV Protease