%0 Journal Article
%T Prevalence of genotypic HIV-1 drug resistance in Thailand, 2002
%A Ekachai Jenwitheesuk
%A Chotip Watitpun
%A Asda Vibhagool
%A Wasun Chantratita
%J Annals of Clinical Microbiology and Antimicrobials
%D 2003
%I BioMed Central
%R 10.1186/1476-0711-2-4
%X Genotypic resistance testing was performed on samples collected in 2002 from 88 HIV-1 infected individuals. Automated DNA sequencing was used to genotype the HIV-1 polymerase gene isolated from patients' plasma.Resistance to protease inhibitors, nucleoside and non-nucleoside reverse transcriptase inhibitors were found in 10 (12%), 42 (48%) and 19 (21%) patients, respectively. The most common drug resistance mutations in the protease gene were at codon 82 (8%), 90 (7%) and 54 (6%), whereas resistant mutations at codon 215 (45%), 67 (40%), 41 (38%) and 184 (27%) were commonly found in the RT gene. This finding indicates that genotypic resistance to nucleoside reverse transcriptase inhibitors was prevalent in 2002. The frequency of resistant mutations corresponding to non-nucleoside reverse transcriptase inhibitors was three times higher-, while resistant mutation corresponding to protease inhibitors was two times lower than those frequencies determined in 2001.This study shows that the frequencies of RT inhibitor resistance mutations have been increased after the reduction in the price of RT inhibitors since December 2001. We believe that this was an important factor that influenced the mutation patterns of HIV-1 protease and RT genes in Thailand.During the last decade, the prevalence of human immunodeficiency virus type 1 (HIV-1) drug resistance has increased in developed countries as a result of widespread antiretroviral therapy [1-9]. Genotypic evidence of resistance for any drug was found in fewer than 2% of cases in one study from 1989 [4], increased to 10%-16% in cohorts recruited after 1995 [2,3], and attained between 20% and 26% in studies performed since 1997 [5-9]. Overall, several studies show rates of primary genotypic drug resistance between 10% and 18% for nucleoside reverse transcriptase inhibitors (NRTIs), of none to 13% for non-nucleoside reverse transcriptase inhibitors (NNRTIs), and of 3% to 7% for protease inhibitors (PIs) [1-9].In July 2002, S Sir
%U http://www.ann-clinmicrob.com/content/2/1/4