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本文引用的文献

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Update of the Drug Resistance Mutations in HIV-1: 2005.2005年HIV-1耐药性突变的更新情况。
Top HIV Med. 2005 Mar-Apr;13(1):51-7.
2
Mutations and polymorphisms associated with antiretroviral drugs in HIV-1C-infected African patients.与HIV-1C感染的非洲患者抗逆转录病毒药物相关的突变和多态性
Antivir Chem Chemother. 2004 Jul;15(4):189-200. doi: 10.1177/095632020401500402.
3
Mutation D30N is not preferentially selected by human immunodeficiency virus type 1 subtype C in the development of resistance to nelfinavir.在对奈非那韦产生耐药性的过程中，1型人类免疫缺陷病毒C亚型不会优先选择D30N突变。
Antimicrob Agents Chemother. 2004 Jun;48(6):2159-65. doi: 10.1128/AAC.48.6.2159-2165.2004.
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Minor mutations in HIV protease at baseline and appearance of primary mutation 90M in patients for whom their first protease-inhibitor antiretroviral regimens failed.
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In vitro hypersusceptibility of human immunodeficiency virus type 1 subtype C protease to lopinavir.1型人类免疫缺陷病毒C亚型蛋白酶对洛匹那韦的体外超敏感性
Antimicrob Agents Chemother. 2003 Sep;47(9):2817-22. doi: 10.1128/AAC.47.9.2817-2822.2003.
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The M184V substitution in human immunodeficiency virus type 1 reverse transcriptase delays the development of resistance to amprenavir and efavirenz in subtype B and C clinical isolates.1型人类免疫缺陷病毒逆转录酶中的M184V替代可延缓B型和C型临床分离株对安普那韦和依非韦伦耐药性的产生。
Antimicrob Agents Chemother. 2003 Jul;47(7):2376-9. doi: 10.1128/AAC.47.7.2376-2379.2003.
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The impact of HIV-1 subtype on the clinical response on HAART.HIV-1亚型对高效抗逆转录病毒治疗临床反应的影响。
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A major role for a set of non-active site mutations in the development of HIV-1 protease drug resistance.一组非活性位点突变在HIV-1蛋白酶耐药性发展中起主要作用。
Biochemistry. 2003 Jan 28;42(3):631-8. doi: 10.1021/bi027019u.
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A V106M mutation in HIV-1 clade C viruses exposed to efavirenz confers cross-resistance to non-nucleoside reverse transcriptase inhibitors.暴露于依非韦伦的HIV-1 C亚型病毒中的V106M突变赋予对非核苷类逆转录酶抑制剂的交叉耐药性。
AIDS. 2003 Jan 3;17(1):F1-5. doi: 10.1097/00002030-200301030-00001.
10
Nelfinavir-resistant, amprenavir-hypersusceptible strains of human immunodeficiency virus type 1 carrying an N88S mutation in protease have reduced infectivity, reduced replication capacity, and reduced fitness and process the Gag polyprotein precursor aberrantly.携带蛋白酶N88S突变的1型人类免疫缺陷病毒的奈非那韦耐药、安普那韦超敏菌株具有降低的感染性、复制能力和适应性，并异常加工Gag多蛋白前体。
J Virol. 2002 Sep;76(17):8659-66. doi: 10.1128/jvi.76.17.8659-8666.2002.

1型人类免疫缺陷病毒C亚型对博茨瓦纳接受含奈非那韦方案治疗失败患者耐药性突变的影响。

Impact of human immunodeficiency virus type 1 subtype C on drug resistance mutations in patients from Botswana failing a nelfinavir-containing regimen.

作者信息

Doualla-Bell Florence, Avalos Ava, Gaolathe Tendani, Mine Madisa, Gaseitsiwe Simani, Ndwapi Ndwapi, Novitsky Vladimir A, Brenner Bluma, Oliveira Maureen, Moisi Daniella, Moffat Howard, Thior Ibou, Essex Max, Wainberg Mark A

机构信息

Botswana-Harvard School of Public Health AIDS Initiative Partnership for HIV Research and Education, Gaborone.

出版信息

Antimicrob Agents Chemother. 2006 Jun;50(6):2210-3. doi: 10.1128/AAC.01447-05.

DOI:10.1128/AAC.01447-05
PMID:16723586
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1479146/
Abstract

Among 16 human immunodeficiency virus-infected (subtype C) Batswana patients who failed nelfinavir (NFV)-containing regimens, the most prevalent mutation observed was D30N (54%), followed by L90M (31%). L89I, K20T/I, and E35D polymorphic changes were also identified. These findings suggest that subtype C viruses in Botswana may develop resistance to NFV via subtype-specific pathways.

摘要

在16例感染人类免疫缺陷病毒（C亚型）且含奈非那韦（NFV）方案治疗失败的博茨瓦纳患者中，观察到最常见的突变是D30N（54%），其次是L90M（31%）。还鉴定出L89I、K20T/I和E35D多态性变化。这些发现表明，博茨瓦纳的C亚型病毒可能通过亚型特异性途径对NFV产生耐药性。