Gea-Banacloche Juan, Johnson Richard T, Bagic Anto, Butman John A, Murray Patrick R, Agrawal Amy Guillet
National Cancer Institute, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.
Ann Intern Med. 2004 Apr 6;140(7):545-53. doi: 10.7326/0003-4819-140-7-200404060-00015.
West Nile virus, a member of the family Flaviviridae, has spread throughout the United States. With more than 9000 cases and 200 deaths in 2003, West Nile virus has become the most common cause of viral encephalitis in several states. West Nile virus encephalitis is a zoonosis. The life cycle of the virus includes mainly birds as hosts and mosquitoes as vectors. Humans are accidental hosts, insufficient to support the life cycle of the virus because of low-grade, transient viremia. However, human-tohuman transmission through blood, organ transplantation, and lactation has been documented. The frequency of severe neurologic disease in the current epidemic suggests a more neurovirulent strain of virus than the one classically associated with West Nile fever. Several neurologic manifestations have been described, but the most characteristic presentation is encephalitis with weakness. Magnetic resonance imaging scans may be normal initially, but a characteristic pattern of involvement of deep gray matter nuclei can be recognized. Although results of polymerase chain reaction may be positive in the cerebrospinal fluid early in the course of the disease, diagnosis is based on serologic tests. Possible cross-reactivity with other members of the genus flavivirus mandates caution when serologic testing results are interpreted. Thus far, no therapeutic intervention has shown consistent clinical efficacy in West Nile virus disease. Several approaches, including interferon-alpha2b and immunoglobulin with high titer against West Nile virus, offer promise based on animal models and limited clinical experience. New drugs with in vitro activity are being investigated, and a vaccine is being developed.
西尼罗河病毒是黄病毒科的一员，已在美国各地传播。2003年，西尼罗河病毒导致了9000多例病例和200人死亡，已成为几个州病毒性脑炎最常见的病因。西尼罗河病毒性脑炎是一种人畜共患病。该病毒的生命周期主要以鸟类为宿主，蚊子为传播媒介。人类是偶然宿主，由于病毒血症程度低且短暂，不足以支持病毒的生命周期。然而，已有文献记载通过血液、器官移植和哺乳进行的人传人传播。当前疫情中严重神经疾病的发生率表明，该病毒株比传统上与西尼罗河热相关的病毒株更具神经毒性。已经描述了几种神经学表现，但最典型的表现是伴有肌无力的脑炎。磁共振成像扫描最初可能正常，但可以识别出深部灰质核受累的特征性模式。尽管在疾病早期脑脊液中的聚合酶链反应结果可能为阳性，但诊断基于血清学检测。在解释血清学检测结果时，由于可能与黄病毒属的其他成员发生交叉反应，因此需要谨慎。迄今为止，尚无治疗干预措施在西尼罗河病毒病中显示出一致的临床疗效。包括干扰素-α2b和高滴度抗西尼罗河病毒免疫球蛋白在内的几种方法，基于动物模型和有限的临床经验显示出前景。正在研究具有体外活性的新药，并正在开发一种疫苗。
