The equine species as Trojan horse for Borna Disease Virus-1?
The equine species as Trojan horse for Borna Disease Virus-1?
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马科动物是博纳病病毒-1 的特洛伊木马吗？
DOI：
10.1080/01652176.2019.1551172
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发表时间：
2018
期刊：
影响因子：
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通讯作者：
J. H. van der Kolk
中科院分区：
文献类型：
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作者：
J. H. van der Kolk
亲爱的读者，最近关于荷兰一名兽医被博尔纳病病毒-1（BoDV-1）血清阳性的马咬伤的报告（Sloet货车Oldruitenborgh-Oosterbaan et al. 2018）引起了人们对该病毒人畜共患病潜力的关注。BoDV-1是大多数哺乳动物博尔纳病病例的原因，是一种在靶细胞核内复制的RNA病毒。它在易感物种中引起严重的，通常是致命的脑炎（Tennis et al. 2016）。最近，德国的3只杂色松鼠（Sciurus variegatoides）饲养者发生脑炎，临床体征相似，并在杂色松鼠1型博纳病毒（VSBV-1）相关临床症状发作后2- 4个月死亡（Hoffmann et al. 2015）。此外，在患有腺室扩张病（PDD）的鹦鹉中，胃肠道重度淋巴浆细胞性神经节炎通常伴有与禽博尔纳病毒（ABV）相关的脑脊髓炎（Staeheli et al. 2010）。这些最近的事件重新引起了人们对这个非凡的病毒家族的兴趣（Tennis et al. 2016）。BoDV是一种有包膜的非节段负链嗜神经性RNA病毒，与狂犬病病毒类似，属于单负链病毒目。博尔纳病最初被描述为马的脑膜脑炎。博尔纳这个名称反映了德国萨克森博尔纳镇附近的疫情，其中大量动物在19世纪末死亡（Lipkin等人，2011）。此外，博尔纳病还在绵羊、牛、美洲驼、猫、狗和鸵鸟中报告。由于实验中感染的物种种类更多，包括兔子、鸟类和灵长类动物，潜在的宿主范围包括所有温血动物。天然BoDV感染主要在欧洲报告（Lipkin和Briese 2007）。值得注意的是，BoDV感染的迹象，包括抗体，抗原，RNA和/或病毒本身，已在许多大陆的动物中报道。然而，动物中最高的临床发病率和经证实的经典博尔纳病病例仅限于中欧（Staeheli et al. 2000; Pawaiya et al. 2010; Kinnunen et al. 2013）。树鼩被认为是BoDV的储存宿主（Hilbe等人，2006年）。马和绵羊博尔纳病的发病率在3月至6月达到峰值（Kinnunen et al. 2013）。由于鼻内感染是有效的，并且自然感染的马的嗅球在病程早期显示出炎症和水肿，因此提出了嗅觉传播途径（Ludwig et al. 1988）。在人类中，1型单纯疱疹病毒（HSV-1）、人类疱疹病毒6型（HHV-6）、博尔纳病病毒、狂犬病病毒和甲型流感病毒也显示可通过嗅觉途径进行神经侵袭（Mori 2015）。在持续几周到几个月的潜伏期后，BoDV感染可引起运动和感觉功能障碍，随后瘫痪和死亡（Richt等人，2000）。马的神经系统病程通常始于兴奋性或抑郁，结束于重度兴奋性、攻击性或嗜睡，以及转圈、轻瘫、麻痹、嗜睡、木僵和昏迷（Kinnunen等人，2013）。对发热（见图1）、厌食和共济失调进行了特征性描述（Katz et al. 1998; Pawaiya et al. 2010; Kinnunen et al. 2013）。还报告了因光感受器丧失而失明（Dietzel等人，2007）和绞痛（Kinnunen等人，2013）。应该认识到，马中的BoDV感染可以存在而没有相关的临床症状。此外，大多数天然BoDV感染未被发现，因为约43%的感染马出现临床疾病（Dieckh 2008）。通过脑内接种用BoDV实验感染的小马在接种后一个月血清转化（Katz等人，1998）。值得注意的是，已经指出感染的动物仅在病毒复制后产生BoDV特异性抗体（Richt和Rott 2001）。随后的神经功能障碍期为脑内注射后3 - 16天，接种后28-30天，2匹小马在这些体征快速发作后死亡（Katz等人，1998）。众所周知的是死后大脑中的特异性Joest-Degen包涵体（Dietzel等人，2007）。狂犬病病毒引起急性致死性脑脊髓炎，仅有轻微的炎性反应，而BoDV感染导致持续性CNS感染，其特征为炎性细胞的大量浸润（Fu等，1993）。此外，狂犬病病毒仅感染神经元，而BoDV也感染神经胶质细胞（Gosztonyi等，1993）。BoDV大分子的核质转运是BoDV生命周期的重要组成部分（De La Torre 2002）。虽然在复制的后期阶段，完整的狂犬病病毒粒子有规律地组装，但BoDV以不完整的形式在中枢神经系统内传播，因此它在形态上保持不可察觉。因此，BoDV只有在离开宿主生物体时才能以完整的包膜形式出现。它仍然没有解决，为什么BoDV容易感染非神经元中枢神经系统
Dear reader, The recent report on a veterinarian bitten by a horse seropositive to Borna Disease Virus-1 (BoDV-1) in the Netherlands (Sloet van Oldruitenborgh-Oosterbaan et al. 2018) draws attention to the zoonotic potential of this virus. BoDV-1, the cause of most cases of mammalian Borna disease, is a RNA virus that replicates within the nucleus of target cells. It causes severe, often lethal, encephalitis in susceptible species (Tizard et al. 2016). Recently, three breeders of variegated squirrels (Sciurus variegatoides) in Germany had encephalitis with similar clinical signs and died 2–4months after onset of the clinical symptoms associated with variegated squirrel 1 Bornavirus (VSBV-1) (Hoffmann et al. 2015). In addition, in psittacine birds with proventricular dilatation disease (PDD) a severe lymphoplasmacytic ganglioneuritis of the gastrointestinal tract is frequently accompanied by encephalomyelitis associated with avian Bornavirus (ABV) (Staeheli et al. 2010). These recent events have revived interest in this remarkable family of viruses (Tizard et al. 2016). BoDV is an enveloped, nonsegmented negativestranded neurotropic RNA virus classified in the virus order Mononegavirales similar to rabies virus. Borna disease was first described as a meningoencephalitis of horses. The name Borna reflects outbreaks in the vicinity of the town Borna, in Saxony, Germany, wherein large numbers of animals died in the late 1800s (Lipkin et al. 2011). Furthermore, Borna disease has also been reported in sheep, cattle, llamas, cats, dogs and ostriches. Because an even larger variety of species has been experimentally infected, including rabbits, birds and primates, the potential host range includes all warm-blooded animals. Natural BoDV infection has been reported primarily in Europe (Lipkin and Briese 2007). Of note, signs of BoDV infection, including antibodies, antigen, RNA and/or virus itself, have been reported from animals in many continents. The highest clinical incidence in animals and the verified classical Borna disease cases, however, are restricted to central Europe (Staeheli et al. 2000; Pawaiya et al. 2010; Kinnunen et al. 2013). Shrews are regarded as reservoir hosts of BoDV (Hilbe et al. 2006). The incidence of Borna disease in horses and sheep peaks in March to June (Kinnunen et al. 2013). An olfactory route for transmission has been proposed because intranasal infection is efficient and the olfactory bulbs of naturally infected horses show inflammation and edema early in the course of disease (Ludwig et al. 1988). In man, herpes simplex virus type 1 (HSV-1), human herpesvirus 6 (HHV-6), Borna disease virus, rabies virus and influenza A virus have also been shown to take the olfactory route for neuroinvasion (Mori 2015). After an incubation period lasting a few weeks to several months, BoDV infection can cause locomotor and sensory dysfunction followed by paralysis and death (Richt et al. 2000). The neurological course in horses usually begins with excitability or depression and ends with severe excitability, aggressiveness or lethargy, and circling, paresis, paralysis, somnolence, stupor and coma (Kinnunen et al. 2013). Fever (see Figure 1), anorexia and ataxia are characteristically described (Katz et al. 1998; Pawaiya et al. 2010; Kinnunen et al. 2013). Blindness due to loss of photoreceptors (Dietzel et al. 2007) and colic have also been reported (Kinnunen et al. 2013). It should be realized that the infection with BoDV in horses can exist without associated clinical symptoms. Furthermore, the majority of natural BoDV infections occur unnoticed as approximately 43% of the infected horses were clinically ill (Dieckh€ ofer 2008). Ponies infected experimentally with BoDV through intracerebral inoculation seroconvert one-month post inoculation (Katz et al. 1998). Of note, it has been stated that infected animals produce BoDVspecific antibodies only after virus replication (Richt and Rott 2001). The ensuing period of neurologic dysfunction ranged from 3 to 16 days following intracerebral injection and two ponies died after rapid onset of these signs 28–30 days post inoculation (Katz et al. 1998). Well known are the pathognomonic Joest-Degen inclusion bodies in the post mortem brains (Dietzel et al. 2007). Rabies virus causes an acute lethal encephalomyelitis with only minor inflammatory reaction, whereas infection with BoDV results in persistent CNS infection characterized by massive infiltration of inflammatory cells (Fu et al. 1993). Furthermore, rabies virus infects only neurons, whereas BoDV also infects glial cells (Gosztonyi et al. 1993). The nucleocytoplasmic transport of BoDV macromolecules is an essential component of the life cycle of BoDV (De La Torre 2002). While in the later phases of replication complete rabies virions are regularly assembled, BoDV propagates within the central nervous system in an incomplete form, so that it remains morphologically imperceptible. Thus, BoDV may appear in a complete, enveloped form only when exiting the host organism. It remains unresolved, why BoDV readily infects non-neuronal central nervous
DOI：
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发表时间：
1993
期刊：
Laboratory investigation; a journal of technical methods and pathology
影响因子：
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作者：
Gosztonyi,G;Dietzschold,B;Kao,M;Rupprecht,CE;Ludwig,H;Koprowski,H
通讯作者：
Koprowski,H