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Clin Infect Dis:首次发现未进行治疗的HIV携带者也会传播耐药性的艾滋病毒

  1. Clin Infect Dis
  2. HIV
  3. 性行为
  4. 携带者
  5. 耐药性

来源:生物谷 2013-11-19 23:45

抵抗艾滋病药物的人类免疫缺陷病毒(HIV)最初是由那些未经过治疗的感染者进行传播的。

2013年11月20日 讯 /生物谷BIOON/ --近日,一项刊登在国际杂志Clinical Infectious Diseases上的一篇研究论文中,来自苏黎世大学医院等处的研究者通过研究表示,抵抗艾滋病药物的人类免疫缺陷病毒(HIV)最初是由那些未经过治疗的感染者进行传播的。为了阻断病毒的传播,必需增加各种抑制措施以及进行早期的HIV诊断显得尤为重要。

在瑞士,每10个HIV携带者中大约就有1个携带者对三种常用于治疗AIDS的药物中的一种产生耐药,而耐药性的病毒最初是通过那些没有经过治疗的患者机体来传播的。

文章中,研究者对1674名发生男男性行为的男性HIV携带者进行了分子流行病学的调查,而且在140名个体中都发现了耐药性的HIV毒株;基于这些男性个体的感染数据以及其血源性病毒的相关性级别,研究者重新构建了这些耐药病毒的传播链,结果发现,大部分在HIV携带者身上发生的耐药病毒的传播都是始于未接受治疗的患者的。

研究者Gunthard表示,我们也很奇怪这些耐药性的病毒最初是来自于未经过治疗的病毒携带者,此前我们研究假设耐药性的毒株是来自那些治疗失败或者正在进行治疗的病毒携带者,可现在的研究结果显然并不是这样。

对于携带耐药性病毒未经过治疗的HIV携带者,显然治疗的措施并不单单依赖于标准化的疗法,而是必须严格抑制这些携带者机体病毒的传播。相比其它检测,比如肝炎检测,HIV检测需要获得病人的许可;而且很多医生都不愿意提及病人的性生活史,这就导致患者的病情被较晚发现。

随着研究的深入,研究者相信未来会开发出更为有效的措施来抑制这些未治疗患者的耐药病毒的传播,以及开发出有效的HIV疗法来对患者进行治疗。(生物谷Bioon.com)

Treatment-Naive Individuals Are the Major Source of Transmitted HIV-1 Drug Resistance in Men Who Have Sex With Men in the Swiss HIV Cohort Study

Sara M. Drescher1, Viktor von Wyl1, Wan-Lin Yang1, Jürg Böni2, Sabine Yerly3, Cyril Shah2, Vincent Aubert4, Thomas Klimkait5, Patrick Taffé6, Hansjakob Furrer7, Manuel Battegay8, Juan Ambrosioni3,9, Matthias Cavassini10, Enos Bernasconi11, Pietro L. Vernazza12, Bruno Ledergerber1, Huldrych F. Günthard1, Roger D. Kouyos1, the Swiss HIV Cohort Study

Background. Human immunodeficiency virus type 1 (HIV-1) transmitted drug resistance (TDR) can compromise antiretroviral therapy (ART) and thus represents an important public health concern. Typically, sources of TDR remain unknown, but they can be characterized with molecular epidemiologic approaches. We used the highly representative Swiss HIV Cohort Study (SHCS) and linked drug resistance database (SHCS-DRDB) to analyze sources of TDR. Methods. ART-naive men who have sex with men with infection date estimates between 1996 and 2009 were chosen for surveillance of TDR in HIV-1 subtype B (N = 1674), as the SHCS-DRDB contains pre-ART genotypic resistance tests for >69% of this surveillance population. A phylogeny was inferred using pol sequences from surveillance patients and all subtype B sequences from the SHCS-DRDB (6934 additional patients). Potential sources of TDR were identified based on phylogenetic clustering, shared resistance mutations, genetic distance, and estimated infection dates. Results. One hundred forty of 1674 (8.4%) surveillance patients carried virus with TDR; 86 of 140 (61.4%) were assigned to clusters. Potential sources of TDR were found for 50 of 86 (58.1%) of these patients. ART-naive patients constitute 56 of 66 (84.8%) potential sources and were significantly overrepresented among sources (odds ratio, 6.43 [95% confidence interval, 3.22–12.82]; P < .001). Particularly large transmission clusters were observed for the L90M mutation, and the spread of L90M continued even after the near cessation of antiretroviral use selecting for that mutation. Three clusters showed evidence of reversion of K103N or T215Y/F. Conclusions. Many individuals harboring viral TDR belonged to transmission clusters with other Swiss patients, indicating substantial domestic transmission of TDR in Switzerland. Most TDR in clusters could be linked to sources, indicating good surveillance of TDR in the SHCS-DRDB. Most TDR sources were ART naive. This, and the presence of long TDR transmission chains, suggests that resistance mutations are frequently transmitted among untreated individuals, highlighting the importance of early diagnosis and treatment.

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