Stone Chris, Ait-Khaled Mounir, Craig Charles, Griffin Philip, Tisdale Margaret
International Clinical Virology, Medicines Research Centre, GlaxoSmithKline Research and Development, Stevenage, Hertfordshire SG1 2NY, United Kingdom.
Antimicrob Agents Chemother. 2004 Apr;48(4):1413-5. doi: 10.1128/AAC.48.4.1413-1415.2004.
Mutations selected or deselected during passage of human immunodeficiency virus strain HXB2 or resistant variants with tenofovir (TFV), abacavir (ABC), and lamivudine (3TC) differed depending on the drug combination and virus genotype. In the wild-type virus, TFV-ABC and TFV-3TC selected K65R (with reduced susceptibility to all three inhibitors) and then Y115F. TFV-containing regimens might increase K65R selection, which confers multiple nucleoside reverse transcriptase inhibitor resistance.
在人类免疫缺陷病毒1型(HIV-1)HXB2毒株或对替诺福韦(TFV)、阿巴卡韦(ABC)和拉米夫定(3TC)耐药的变异株传代过程中选择或未选择的突变,因药物组合和病毒基因型而异。在野生型病毒中,TFV-ABC和TFV-3TC选择了K65R(对所有三种抑制剂的敏感性降低),然后是Y115F。含TFV的治疗方案可能会增加K65R的选择,这会导致对多种核苷类逆转录酶抑制剂耐药。