HERPES SIMPLEX--PREGNANCY, NEONATAL RISK, HOST DEFENSE

单纯疱疹——妊娠、新生儿风险、宿主防御

• 批准号: 3146908
• 负责人: CHARLES G PROBER
• 金额: $ 24.8万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1991
• 资助国家: 美国
• 起止时间: 1991-09-15 至 1995-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3146908
• 关键词: Herpesviridae disease; amniotic fluid; antibody formation; antiviral agents; communicable disease control; communicable disease transmission; disease /disorder proneness /risk; female; genital herpes; glycoproteins; herpes simplex virus 1; herpes simplex virus 2; human pregnant subject; human subject; infant human (0-1 year); leukocyte activation /transformation; microorganism disease chemotherapy; microorganism immunology; neutralizing antibody; newborn human (0-6 weeks); pregnancy immunology; prenatal diagnosis; rapid diagnosis; relapse /recurrence; serotyping; sexually transmitted diseases; virus antigen; virus classification; virus infection mechanism; virus protein

The incidence of neonatal HSV infections is increasing in parallel with the increase in genital HSV infections. Preventing most cases of neonatal HSV infections depends upon avoiding contact with the virus at delivery. If lesions are present, delivery by cesarean section is indicated. Unfortunately, most neonatal infections result from exposure to asymptomatic maternal excretion of HSV, often by women with no past history of genital herpes. The failure of antepartum cultures to predict asymptomatic shedding at delivery in women with past recurrent genital herpes along with the fact that many mothers of infants with neonatal HSV have no history of genital herpes requires another approach to the problem of neonatal HSV. Most genital HSV infections are caused by HSV-2. Seroepidemiologic studies have been hampered by cross-reactivity between HSV-1 and 2 antigens until the development of serologic methods which detect antibodies to HSV-2 specific glycoproteins. We propose to investigate the value of taking viral cultures for HSV at all deliveries, regardless of maternal herpes history, and of HSV-2 specific serologic testing early and late in gestation. Past or recent HSV-2 infection will be determined by testing paired sera from the first prenatal visit and 28-32 weeks gestation using an ELISA method to detect antibodies to the HSV-2 glycoprotein G, which has HSV-2 specific epitopes. The frequency of HSV-2 infections in consecutive pregnant women with or without a history of genital HSV and the proportion which are primary infections will be assessed. Cultures will be obtained from all mothers and infants at delivery (approximately 5000/year). The sensitivity and specificity of shell vial culture and HSV antigen detection by enzyme immunofiltration for rapid diagnosis of neonatal HSV exposure will be compared with a standard tissue culture technique. The frequency of asymptomatic shedding of HSV at delivery among women with or without serologic evidence of past or recent HSV-2 infections will be determined. The frequency of prematurity, low birth weight, and/or evidence of intrauterine HSV infections among neonates born to mothers with serologic evidence of HSV-2 infections will be assessed. Much of the continued morbidity and mortality of neonatal HSV is due to delayed diagnosis. While delivery cultures will not prevent the exposure of infants to asymptomatic maternal HSV, identification of exposed infants should allow early diagnosis and immediate antiviral therapy of neonatal HSV. Infants known to be exposed to asymptomatic maternal HSV will be monitored to determine the frequency of subclinical and clinical HSV infections. Exposed neonates who do not contract HSV will be compared with HSV- infected neonates referred during the study period using assays for HSV neutralizing antibody, antibody mediating cellular cytotoxicity and antibodies to HSV glycoproteins. The failure of antepartum cultures to predict and therefore prevent neonatal exposures to HSV at delivery has made it critical to develop a rational approach to the problem of neonatal HSV infections.

新生儿单纯疱疹病毒感染的发病率正在平行增加 生殖器HSV感染的增加。 阻止大部分 新生儿HSV感染病例取决于避免接触 在分娩时携带病毒 如果存在病变，则通过 剖腹产是指征。 不幸的是，大多数新生儿 接触无症状产妇导致感染 HSV排泄，通常由没有生殖器感染史的女性进行 疱疹 产前培养未能预测 既往复发性阴道炎妇女分娩时无症状脱落 生殖器疱疹沿着的事实是，许多婴儿的母亲 生殖器疱疹的危害有哪些？ 解决新生儿单纯疱疹病毒问题的另一种方法。 大多数生殖器 HSV感染由HSV-2引起。 血清流行病学研究 HSV-1和HSV-2之间的交叉反应性阻碍了 抗原，直到血清学方法的发展， HSV-2特异性糖蛋白的抗体。 我们建议 研究HSV病毒培养的价值 分娩，无论母亲疱疹史，和HSV-2 在妊娠早期和晚期进行特异性血清学检测。 过去或 最近HSV-2感染将通过检测配对血清来确定 从第一次产前检查和妊娠28-32周开始， ELISA方法检测HSV-2糖蛋白G的抗体， 其具有HSV-2特异性表位。 HSV-2的频率 有或没有感染的连续怀孕妇女 生殖器HSV病史和原发性比例 将对感染进行评估。 培养物将从所有 分娩时的母亲和婴儿（约5 000人/年）。 的 壳瓶培养和HSV抗原敏感性和特异性 酶免疫过滤法快速诊断 将新生儿HSV暴露与标准组织进行比较 培养技术 无症状脱落的频率 有或无血清学证据的女性分娩时的单纯疱疹病毒 将确定过去或最近的HSV-2感染。 的 早产、低出生体重和/或 孕妇所生新生儿的宫内单纯疱疹病毒感染 将评估HSV-2感染的血清学证据。 大部分 新生儿HSV的持续发病率和死亡率是由于 延误诊断 虽然交付文化不会阻止 婴儿暴露于无症状的母体单纯疱疹病毒，鉴定 暴露的婴儿应允许早期诊断和立即 新生儿HSV的抗病毒治疗。 已知暴露于 将监测无症状的母体HSV，以确定 亚临床和临床HSV感染的频率。 暴露 未感染HSV的新生儿将与HSV进行比较- 研究期间使用检测试剂盒转诊的感染新生儿 对于HSV中和抗体，抗体介导细胞 细胞毒性和抗HSV糖蛋白的抗体。 的失败 产前培养以预测并预防新生儿 在分娩时暴露于HSV使得开发一种 新生儿HSV感染问题的合理方法。