Department of Immunobiology, College of Medicine, University of Arizona, Tucson, AZ, United States.
Life Sci. 2011 May 23;88(21-22):980-6. doi: 10.1016/j.lfs.2010.09.023. Epub 2010 Oct 1.
HIV-1 mother-to-child transmission (MTCT) occurs mainly at three stages, including prepartum, intrapartum and postpartum. Several maternal factors, including low CD4+ lymphocyte counts, high viral load, immune response, advanced disease status, smoking and abusing drugs have been implicated in an increased risk of HIV-1 MTCT. While use of antiretroviral therapy (ART) during pregnancy has significantly reduced the rate of MTCT, selective transmission of ART resistant mutants has been reported. Based on HIV-1 sequence comparison, the maternal HIV-1 minor genotypes with R5 phenotypes are predominantly transmitted to their infants and initially maintained in the infants with the same properties. Several HIV-1 structural, regulatory and accessory genes were highly conserved following MTCT. In addition, HIV-1 sequences from non-transmitting mothers are less heterogeneous compared with transmitting mothers, suggesting that a higher level of viral heterogeneity influences MTCT. Analysis of the immunologically relevant epitopes showed that variants evolved to escape the immune response that influenced HIV-1 MTCT. Several cytotoxic T-lymphocyte (CTL) epitopes were identified in various HIV-1 genes that were conserved in HIV-1 mother-infant sequences, suggesting a role in MTCT. We have shown that HIV-1 replicates more efficiently in neonatal T-lymphocytes and monocytes/macrophages compared with adult cells, and this differential replication is influenced at the level of HIV-1 gene expression, which was due to differential expression of host factors, including transcriptional activators, signal transducers and cytokines in neonatal than adult cells. In addition, HIV-1 integration occurs in more actively transcribed genes in neonatal compared with adult cells, which may influence HIV-1 gene expression. The increased HIV-1 gene expression and replication in neonatal target cells contribute to a higher viral load and more rapid disease progression in neonates/infants than adults. These findings may identify targets, viral and host, for developing strategies for HIV-1 prevention and treatment.
HIV-1 母婴传播(MTCT)主要发生在三个阶段,包括产前、产时和产后。一些母体因素,包括低 CD4+淋巴细胞计数、高病毒载量、免疫反应、疾病进展、吸烟和吸毒,与 HIV-1 MTCT 的风险增加有关。虽然在怀孕期间使用抗逆转录病毒疗法(ART)显著降低了 MTCT 的发生率,但已有报道称选择传播 ART 耐药突变体。基于 HIV-1 序列比较,具有 R5 表型的母体 HIV-1 次要基因型主要传播给婴儿,并最初以相同的特性在婴儿中维持。在 MTCT 后,几个 HIV-1 结构、调节和辅助基因高度保守。此外,与传播母亲相比,非传播母亲的 HIV-1 序列的异质性较低,这表明更高水平的病毒异质性影响 MTCT。免疫相关表位分析表明,变异体进化以逃避影响 HIV-1 MTCT 的免疫反应。在各种 HIV-1 基因中鉴定出几个细胞毒性 T 淋巴细胞(CTL)表位,这些表位在 HIV-1 母婴序列中保守,提示其在 MTCT 中发挥作用。我们已经表明,与成人细胞相比,HIV-1 在新生儿 T 淋巴细胞和单核细胞/巨噬细胞中的复制效率更高,这种差异复制受 HIV-1 基因表达水平的影响,这是由于转录因子、信号转导和细胞因子等宿主因子在新生儿细胞中比成人细胞中的差异表达所致。此外,与成人细胞相比,HIV-1 整合发生在新生儿细胞中更活跃转录的基因中,这可能影响 HIV-1 基因表达。新生儿靶细胞中 HIV-1 基因表达和复制的增加导致新生儿/婴儿的病毒载量更高,疾病进展更快,比成人更快。这些发现可能确定了用于开发 HIV-1 预防和治疗策略的目标、病毒和宿主。