人免疫缺陷病毒包膜蛋白在母婴传播过程中的作用
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摘要
I型人免疫缺陷病毒(HIV-1)母婴传播(MTCT)的现象在资源匮乏的地区仍然是个很严重的问题。在医疗并不发达的非洲撒哈拉以南地区尤为突出，15岁以下感染HIV-1的儿童超过90%都生活在这里，并且新感染HIV-1的患儿超过95%都在这里。此外，在这个地区C亚型HIV-1最为流行，其感染率已经超过60%。由于目前尚未存在预防MTCT的有效疫苗及这些发展中国家的抗病毒药物并不普及，因此探究MTCT过程中优先传播病毒的生物学特征对找到阻断MTCT的有效策略具有重要意义。
我们前期研究表明在慢性感染母婴对中传播到婴儿的病毒和母亲的病毒相比具有更高的复制适应性，并且这个特征是由HIV-1包膜糖蛋白(Env)的V1-V5区决定的。为了确定慢性感染母婴对中传播病毒的高复制适应性是否由Env V1-V5区诱导了更高的病毒进入效率导致的，利用两种不同的研究Env介导细胞间融合的方法，对5对慢性感染和2对急性感染母婴对中母亲和婴儿病毒Env V1-V5区诱导细胞融合的能力进行了比较分析。结果表明，在1对慢性感染母婴对中发现了婴儿病毒Env V1-V5区具有更高的介导细胞融合的能力并且是由V4V5区决定的，而在其他母婴对中未得到一致的趋势和明显的差异。这些结果表明在HIV-1母婴传播过程中传播病毒的复制适应性和其Env V1-V5区诱导的进入效率并无显著的正相关性。母婴传播的方式和时间也可能参与影响病毒复制适应性的选择。
对感染HIV-1的孕妇及新生儿进行抗病毒药物的治疗与预防能够有效的降低HIV-1的MTCT，但是随之带来的病毒耐药性问题也引起了人们的关注。小分子的CCR5拮抗剂代表了一类新的治疗HIV-1感染的药物。Maraviroc是这类药物中唯一被FDA批准的多应用于被R5嗜性病毒感染但对多种抗病毒药物出现耐药性的患者治疗中，并于最近批准进入一线临床药物。虽然病毒中存在的maraviroc原发性耐药位点会影响maraviroc将来在阻断MTCT中的临床应用，但对于maraviroc原发性耐药位点在母婴传播样本中的流行及传播鲜有报道。
为了评价maraviroc原发性耐药位点在本文母婴传播样本中的流行及传播，并且分析各母婴对Env对maraviroc的敏感性，对6对慢性感染和3对急性感染母婴对Env进行了序列分析检测maraviroc原发性耐药位点的流行及传播，同时也分析了已有报道的另一种小分子CCR5拮抗剂-vicriviroc的原发性耐药位点。将其中4对慢性和2对急性感染母婴对Env构建到病毒骨架中形成重组病毒评价其对maraviroc的敏感性。结果表明Env中A316T突变（赋予对maraviroc的部分抗性）、T307I和R315Q突变（赋予对vicriviroc的部分抗性）在各母婴对母亲和婴儿病毒准种群中流行率很高，意味着母亲病毒准种群中的原发性耐药位点可以随母婴传播过程传播到婴儿。但传播的方式在急性感染和慢性感染样本中是有区别的，在急性感染样本中，在母亲中存在的突变位点趋于以复制的形式直接从母亲传到婴儿，而在慢性感染样本中，一些低频率的突变位点在母婴传播过程中丢失，只有高频率（接近100%）的突变位点才会被传播下来。此外，样本中母亲和婴儿病毒对maraviroc均敏感，但慢性感染样本中母亲和婴儿病毒比急性感染样本中母亲和婴儿病毒对maravirocc更为敏感。
这些结果表明在母婴传播中原发性耐药位点的传播方式及样本对maraviroc的敏感性依赖于样本的感染类型，同时maraviroc在临床应用上对急性感染母婴对群体的应用剂量要高于慢性感染母婴对。
Mother-to-child transmission(MTCT) of the humanimmunodeficiency virus type1(HIV-1) remains a significant problem inthe resource-constrained settings. This is especially worse in sub-SaharanAfrica where more than90%of the infected children under the age of15are living and the majority (95%) of new pediatric infections occurred,and where therapeutic intervention is still not widely available. Moreover,the HIV-1subtype C is the most prevalent and account for more than60%of infections in that epidemic region. Given the absence of aprophylactic vaccine or universal access to preventive treatment in thesedeveloping countries, a clear understanding of the characteristics ofpreferentially transmitted viruses is critical to the development ofeffective measures to reduce rates of MTCT.
Our previous study demonstrated that the newly transmitted viruses (in infant) of chronically infected mother-infant pairs (MIPs) were morefit in growth, as imparted by their envelope glycoproteins V1-V5regions,than those in their corresponding chronically infected mothers. In orderto investigate whether the higher fitness of transmitted viruses wasconferred by their higher entry efficiency directed by the V1-V5regionsduring perinatal transmission, we analyzed the fusogenicity of Envcontaining V1-V5regions derived from transmitted andnon-tranmsmitted viruses of five chronically infected MIPs and twoacutely infected MIPs via two different cell-to-cell fusion assays. Theresults showed that higher fusion efficiency induced by infant EnvV1-V5than their corresponding mothers was observed in one chronicallyinfected MIP. Moreover, the V4V5regions play an important role todiscriminate the transmitted and non-transmitted viruses in this pair.However, neither consistent pattern nor significant differences offusogenicity mediated by V1-V5regions between maternal and infant variants was observed in other MIPs. Our study suggests that there is noconsistent and significant correlation between viral fitness selection andentry efficiency directed by V1-V5regions during perinatal transmission.Other factors such as the route and timing of transmission may also beinvolved.
Antiretroviral drugs (ARVs) for HIV-1-infected pregnant women andtheirinfants are highly effective in reducing MTCT of HIV-1, whereasconcerns have been raised about the public health implications of theemergence of resistance to antiretroviral drugs. Small molecular CCR5inhibitors represent a new class of drugs for treating HIV-1infection.Maraviroc was the only CCR5antagonist approved by the FDA to beutilized as a salvage therapy for multi-drug resistant patients with R5tropic virus but has been recently approved for first-line treatmentregimens. No studies have evaluated the prevalence and transmission ofnaturally occurring mutations associated with maraviroc during peranatal transmission since they may have a profound impact on the clinicalmanagement of maraviroc in MTCT in future.
To evaluate the prevalence and transmission of natural resistancemutations to maraviroc during peranatal transmission and analyze thesensitivity of mother-infant pairs to maraviroc, six chronically infectedMIPs and three acutely infected MIPs were recruited to analyze theprevalence and transmission of natural resistance mutations to maravirocand another small molecular CCR5antagonist-vicriviroc. And fourrepresentative chronically infected MIPs and two acutely infected MIPswere employed to construct provirus clones and to analyze the sensitivityto maraviroc. Mutations A316T, conferring partial resistance tomaraviroc, and T307I and R315Q, both conferring partial resistance tovicriviroc are prevalent in mother and infant cohorts of either acutelyinfected MIPs or chronically infected MIPs, indicating the transmissionof natural resistance mutations during peranatal transmission. The mutations present at viral quasispecies of acutely infected mothers seemto directly transmit to their corresponding infants, while some mutationsespecially at low frequency of chronically infected mothers would be lostduring transmission except the very high frequency. Moreover, thesensitivities to maraviroc of maternal and infant viruses of acutelyinfected MIPs are less susceptive than chronically infected MIPsrespectively.
Our study suggests that the transmission mode of natural resistancemutations and the sensitivity to maraviroc are dependent on infectionstate of MIPs either acutely infected or chronically infected. These resultsmay indicate that higher dose of maraviroc is indispensable for treatmentof acutely infected MIPs compared to chronically infected MIPs.
我们前期研究表明在慢性感染母婴对中传播到婴儿的病毒和母亲的病毒相比具有更高的复制适应性，并且这个特征是由HIV-1包膜糖蛋白(Env)的V1-V5区决定的。为了确定慢性感染母婴对中传播病毒的高复制适应性是否由Env V1-V5区诱导了更高的病毒进入效率导致的，利用两种不同的研究Env介导细胞间融合的方法，对5对慢性感染和2对急性感染母婴对中母亲和婴儿病毒Env V1-V5区诱导细胞融合的能力进行了比较分析。结果表明，在1对慢性感染母婴对中发现了婴儿病毒Env V1-V5区具有更高的介导细胞融合的能力并且是由V4V5区决定的，而在其他母婴对中未得到一致的趋势和明显的差异。这些结果表明在HIV-1母婴传播过程中传播病毒的复制适应性和其Env V1-V5区诱导的进入效率并无显著的正相关性。母婴传播的方式和时间也可能参与影响病毒复制适应性的选择。
对感染HIV-1的孕妇及新生儿进行抗病毒药物的治疗与预防能够有效的降低HIV-1的MTCT，但是随之带来的病毒耐药性问题也引起了人们的关注。小分子的CCR5拮抗剂代表了一类新的治疗HIV-1感染的药物。Maraviroc是这类药物中唯一被FDA批准的多应用于被R5嗜性病毒感染但对多种抗病毒药物出现耐药性的患者治疗中，并于最近批准进入一线临床药物。虽然病毒中存在的maraviroc原发性耐药位点会影响maraviroc将来在阻断MTCT中的临床应用，但对于maraviroc原发性耐药位点在母婴传播样本中的流行及传播鲜有报道。
为了评价maraviroc原发性耐药位点在本文母婴传播样本中的流行及传播，并且分析各母婴对Env对maraviroc的敏感性，对6对慢性感染和3对急性感染母婴对Env进行了序列分析检测maraviroc原发性耐药位点的流行及传播，同时也分析了已有报道的另一种小分子CCR5拮抗剂-vicriviroc的原发性耐药位点。将其中4对慢性和2对急性感染母婴对Env构建到病毒骨架中形成重组病毒评价其对maraviroc的敏感性。结果表明Env中A316T突变（赋予对maraviroc的部分抗性）、T307I和R315Q突变（赋予对vicriviroc的部分抗性）在各母婴对母亲和婴儿病毒准种群中流行率很高，意味着母亲病毒准种群中的原发性耐药位点可以随母婴传播过程传播到婴儿。但传播的方式在急性感染和慢性感染样本中是有区别的，在急性感染样本中，在母亲中存在的突变位点趋于以复制的形式直接从母亲传到婴儿，而在慢性感染样本中，一些低频率的突变位点在母婴传播过程中丢失，只有高频率（接近100%）的突变位点才会被传播下来。此外，样本中母亲和婴儿病毒对maraviroc均敏感，但慢性感染样本中母亲和婴儿病毒比急性感染样本中母亲和婴儿病毒对maravirocc更为敏感。
这些结果表明在母婴传播中原发性耐药位点的传播方式及样本对maraviroc的敏感性依赖于样本的感染类型，同时maraviroc在临床应用上对急性感染母婴对群体的应用剂量要高于慢性感染母婴对。
Mother-to-child transmission(MTCT) of the humanimmunodeficiency virus type1(HIV-1) remains a significant problem inthe resource-constrained settings. This is especially worse in sub-SaharanAfrica where more than90%of the infected children under the age of15are living and the majority (95%) of new pediatric infections occurred,and where therapeutic intervention is still not widely available. Moreover,the HIV-1subtype C is the most prevalent and account for more than60%of infections in that epidemic region. Given the absence of aprophylactic vaccine or universal access to preventive treatment in thesedeveloping countries, a clear understanding of the characteristics ofpreferentially transmitted viruses is critical to the development ofeffective measures to reduce rates of MTCT.
Our previous study demonstrated that the newly transmitted viruses (in infant) of chronically infected mother-infant pairs (MIPs) were morefit in growth, as imparted by their envelope glycoproteins V1-V5regions,than those in their corresponding chronically infected mothers. In orderto investigate whether the higher fitness of transmitted viruses wasconferred by their higher entry efficiency directed by the V1-V5regionsduring perinatal transmission, we analyzed the fusogenicity of Envcontaining V1-V5regions derived from transmitted andnon-tranmsmitted viruses of five chronically infected MIPs and twoacutely infected MIPs via two different cell-to-cell fusion assays. Theresults showed that higher fusion efficiency induced by infant EnvV1-V5than their corresponding mothers was observed in one chronicallyinfected MIP. Moreover, the V4V5regions play an important role todiscriminate the transmitted and non-transmitted viruses in this pair.However, neither consistent pattern nor significant differences offusogenicity mediated by V1-V5regions between maternal and infant variants was observed in other MIPs. Our study suggests that there is noconsistent and significant correlation between viral fitness selection andentry efficiency directed by V1-V5regions during perinatal transmission.Other factors such as the route and timing of transmission may also beinvolved.
Antiretroviral drugs (ARVs) for HIV-1-infected pregnant women andtheirinfants are highly effective in reducing MTCT of HIV-1, whereasconcerns have been raised about the public health implications of theemergence of resistance to antiretroviral drugs. Small molecular CCR5inhibitors represent a new class of drugs for treating HIV-1infection.Maraviroc was the only CCR5antagonist approved by the FDA to beutilized as a salvage therapy for multi-drug resistant patients with R5tropic virus but has been recently approved for first-line treatmentregimens. No studies have evaluated the prevalence and transmission ofnaturally occurring mutations associated with maraviroc during peranatal transmission since they may have a profound impact on the clinicalmanagement of maraviroc in MTCT in future.
To evaluate the prevalence and transmission of natural resistancemutations to maraviroc during peranatal transmission and analyze thesensitivity of mother-infant pairs to maraviroc, six chronically infectedMIPs and three acutely infected MIPs were recruited to analyze theprevalence and transmission of natural resistance mutations to maravirocand another small molecular CCR5antagonist-vicriviroc. And fourrepresentative chronically infected MIPs and two acutely infected MIPswere employed to construct provirus clones and to analyze the sensitivityto maraviroc. Mutations A316T, conferring partial resistance tomaraviroc, and T307I and R315Q, both conferring partial resistance tovicriviroc are prevalent in mother and infant cohorts of either acutelyinfected MIPs or chronically infected MIPs, indicating the transmissionof natural resistance mutations during peranatal transmission. The mutations present at viral quasispecies of acutely infected mothers seemto directly transmit to their corresponding infants, while some mutationsespecially at low frequency of chronically infected mothers would be lostduring transmission except the very high frequency. Moreover, thesensitivities to maraviroc of maternal and infant viruses of acutelyinfected MIPs are less susceptive than chronically infected MIPsrespectively.
Our study suggests that the transmission mode of natural resistancemutations and the sensitivity to maraviroc are dependent on infectionstate of MIPs either acutely infected or chronically infected. These resultsmay indicate that higher dose of maraviroc is indispensable for treatmentof acutely infected MIPs compared to chronically infected MIPs.
引文
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