High frequency of drug resistance mutations in human immunodeficiency virus type 1-infected Korean patients treated with HAART.

We have investigated the frequency of resistance mutations to highly active antiretroviral therapy (HAART) in 37 Korean HIV-1-infected patients, 22 of whom had experienced previous monotherapy. CD4(+) T cell counts significantly increased from 135 +/- 110/microl to 523 +/- 259/microl for 39 +/- 3 months by HAART (p < 0.0001). Over 39 +/- 3 months of HAART, 18 of 37 patients (48.6%) harbored drug resistance mutations. The most frequently observed mutation was M184V (24.3%, 9/37). Seven of 35 patients (20.0%) exposed to protease inhibitors and 2 of 11 (18.2%) exposed to nonnucleoside reverse transcriptase inhibitors developed resistance mutations to their respective drugs. When we measured HIV-1 RNA viral loads over 30 months of HAART in 31 patients, we found that 13 patients (41.9%) showed virological treatment failure, with viral load >400 copies/ml. In conclusion, we found that the frequency of resistance mutations to antiretroviral drugs over 30 months was high in HAART-treated patients. As the first report on resistance mutations to HAART in Korea, our data suggest that genotyping-guided treatment as well as education for compliance are required for better care.

High frequency of grossly deleted nef genes in HIV-1 infected long-term slow progressors treated with Korean red ginseng.

To investigate the association between Korean red ginseng (KRG) intake in HIV-1 infected patients and the occurrence of grossly deleted nef genes (gDeltanef), we characterized nef genes in 10 long-term slow progressors (LTSP) infected with HIV-1 subtype B and 34 control patients. LTSP was defined by the annual decrease in CD4 T cells being less than 20/microl over 10 years in the absence of antiretroviral therapy. They were treated with KRG for a prolonged period. Nef genes were amplified from peripheral blood mononuclear cells (PBMC) using nested PCR and the products were sequenced directly. It was observed that the patients CD4 T cell counts decreased from 444 +/- 207/microl to 294 +/- 177/microl over 136 +/- 23 months of KRG intake. This corresponds to an annual decrease in the level of CD4 T cells of 13.3/microl. A total of 479 nef genes were amplified from 137 PBMC samples. Nine out of the 10 patients, 47 (34.3%) out of the 137 samples, and 90 out of the 479 genes revealed gDeltanef. The deletion extended outside the nef gene in 25 gDeltanef obtained from 6 patients. The proportion of samples with gDeltanef (34.3%) was significantly higher than 4.8% in control patients (P < 0.001). In addition, it significantly increased as the duration of KRG intake prolongs (P < 0.01). These data suggest that the occurrence of gDeltanef might be associated with long-term intake of KRG.