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首页> 外文期刊>Emerging Infectious Diseases >Lack of Serologic Evidence for an Association between Cache Valley Virus Infection and Anencephaly and other Neural Tube Defects in Texas
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Lack of Serologic Evidence for an Association between Cache Valley Virus Infection and Anencephaly and other Neural Tube Defects in Texas

机译:缺乏血清学证据,证明德克萨斯州的缓存谷病毒感染与无脑和其他神经管缺陷之间存在关联

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We tested the hypothesis that Cache Valley Virus (CVV), an endemic North American bunyavirus, may be involved in the pathogenesis of human neural tube defects. This investigation followed a 1990 and 1991 south Texas outbreak of neural tube defects with a high prevalence of anencephaly and the demonstration in 1987 that in utero infection by CVV was the cause of outbreaks of central nervous system and musculoskeletal defects in North American ruminants. Sera from 74 women who gave birth to infants with neural tube defects in south Texas from 1993 through early 1995 were tested for CVV neutralizing antibody. All tested sera did not neutralize CVV. These data suggest that CVV is not involved in the induction of human neural tube defects during nonepidemic periods but do not preclude CVV involvement during epidemics. Other endemic bunyaviruses may still be involved in the pathogenesis of neural tube defects or other congenital central nervous system or musculoskeletal malformations.
机译:我们测试了一种假说:北美流行的布尼亚病毒Cache Valley病毒(CVV)可能与人类神经管缺陷的发病机制有关。这项调查是在1990年和1991年在得克萨斯州南部爆发神经管缺陷且无脑流行率很高,1987年的一次证明表明,CVV在子宫内感染是北美反刍动物爆发中枢神经系统和肌肉骨骼缺陷的原因。测试了1993年至1995年初在得克萨斯州南部出生的74例患有神经管缺陷婴儿的妇女的血清CVV中和抗体。所有测试的血清均未中和CVV。这些数据表明,在非流行期间,CVV不参与人类神经管缺陷的诱导,但不排除在流行期间CVV参与。其他地方性布尼亚病毒仍可能参与神经管畸形或其他先天性中枢神经系统或肌肉骨骼畸形的发病机制。

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