Farquhar Carey, Nduati Ruth, Haigwood Nancy, Sutton William, Mbori-Ngacha Dorothy, Richardson Barbra, John-Stewart Grace
Department of Medicine, University of Washington, Seattle, WA 98104-2499, USA.
J Acquir Immune Defic Syndr. 2005 Dec 1;40(4):494-7. doi: 10.1097/01.qai.0000168179.68781.95.
Studies among HIV-1-infected women have demonstrated reduced placental transfer of IgG antibodies against measles and other pathogens. As a result, infants born to women with HIV-1 infection may not acquire adequate passive immunity in utero and this could contribute to high infant morbidity and mortality in this vulnerable population.
To determine factors associated with decreased placental transfer of measles IgG, 55 HIV-1-infected pregnant women who were enrolled in a Nairobi perinatal HIV-1 transmission study were followed. Maternal CD4 count, HIV-1 viral load, and HIV-1-specific gp41 antibody concentrations were measured antenatally and at delivery. Measles IgG concentrations were assayed in maternal blood and infant cord blood obtained during delivery to calculate placental antibody transfer.
Among 40 women (73%) with positive measles titers, 30 (75%) were found to have abnormally low levels of maternofetal IgG transfer (<95%). High maternal HIV-1 viral load at 32 weeks' gestation and at delivery was associated with reductions in placental transfer (P < 0.0001 and P = 0.0056, respectively) and infant measles IgG concentrations in cord blood (P < 0.0001 and P = 0.0073, respectively). High maternal HIV-1-specific gp41 antibody titer was also highly correlated with both decreased placental transfer (P = 0.0080) and decreased infant IgG (P < 0.0001).
This is the first study to evaluate the relationship between maternal HIV-1 viremia, maternal HIV-1 antibody concentrations, and passive immunity among HIV-1-exposed infants. These data support the hypothesis that high HIV-1 viral load during the last trimester may impair maternofetal transfer of IgG and increases risk of measles and other serious infections among HIV-1-exposed infants.
针对感染人类免疫缺陷病毒1型（HIV-1）女性的研究表明，针对麻疹和其他病原体的IgG抗体的胎盘转运减少。因此，感染HIV-1的女性所生婴儿在子宫内可能无法获得足够的被动免疫，这可能导致这一脆弱人群中婴儿的高发病率和高死亡率。
为了确定与麻疹IgG胎盘转运减少相关的因素，对参加内罗毕围产期HIV-1传播研究的55名感染HIV-1的孕妇进行了随访。在产前和分娩时测量孕妇的CD4细胞计数、HIV-1病毒载量以及HIV-1特异性糖蛋白41（gp41）抗体浓度。检测分娩时采集的孕妇血液和婴儿脐带血中的麻疹IgG浓度，以计算胎盘抗体转运情况。
在40名麻疹滴度呈阳性的女性（73%）中，有30名（75%）的母婴IgG转运水平异常低（<95%）。妊娠32周时和分娩时孕妇的高HIV-1病毒载量与胎盘转运减少相关（分别为P<0.0001和P = 0.0056），以及脐带血中婴儿麻疹IgG浓度降低相关（分别为P<0.0001和P = 0.0073）。孕妇的高HIV-1特异性gp41抗体滴度也与胎盘转运减少（P = 0.0080）和婴儿IgG降低（P<0.0001）高度相关。
这是第一项评估孕妇HIV-1病毒血症、孕妇HIV-1抗体浓度与暴露于HIV-1的婴儿被动免疫之间关系的研究。这些数据支持以下假设：妊娠晚期的高HIV-1病毒载量可能会损害IgG的母婴转运，并增加暴露于HIV-1的婴儿患麻疹和其他严重感染的风险。
