Department of Microbiology, Western College of Veterinary Microbiology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Wildlife Rehab Society of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Transbound Emerg Dis. 2019 Mar;66(2):1054-1062. doi: 10.1111/tbed.13102. Epub 2018 Dec 26.
Many viruses that cause serious and often fatal disease in humans have spilled over from bats. Recent evidence suggests that stress may enhance virus shedding by bats increasing the possibility of transmission to other species. To understand the reasons for spillover is therefore important to determine the molecular pathways that link stress to virus reactivation and shedding in bats. We recently isolated and characterized a gammaherpesvirus (Eptesicus fuscus herpesvirus, EfHV) autochthonous to North American big brown bats. Since herpesviruses are known to reactivate from latent infections in response to a wide variety of stressors, EfHV presents us with an opportunity to study how physiological, behavioural or environmental changes may influence the big brown bats' relationship with EfHV. To understand the biology of the virus and how the extended periods of torpor experienced by these bats during hibernation along with the stress of arousal might influence the virus-host relationship, we attempted to detect the virus in the blood of wild-caught non-hibernating bats as well as captive bats arising from hibernation. We compared the prevalence of EfHV in the blood (using PCR) and EfHV-specific antibodies (using ELISA) between captive hibernating bats and wild-caught non-hibernating bats. We detected EfHV only in the blood of captive hibernating bats (27.8% = 10/36) and not in wild-caught non-hibernating bats (0.0% = 0/43). In contrast, the EfHV-specific antibody titres were higher in the non-hibernating bats compared to the hibernating bats. Our study suggests that: (a) viral DNA in blood indicates reactivation from latency, (b) long periods of hibernation lead to suppression of immunity, (c) stress of arousal from hibernation reactivates the virus in bats with lower levels of anti-viral immunity (indicated by humoral immune response), and (d) levels of anti-viral immunity increase in non-hibernating bats following reactivation.
许多导致人类严重甚至致命疾病的病毒已从蝙蝠传播给人类。最近的证据表明，压力可能通过增加病毒向其他物种传播的可能性来增强蝙蝠的病毒脱落。因此，了解病毒溢出的原因对于确定将压力与蝙蝠中病毒的重新激活和脱落联系起来的分子途径很重要。我们最近从北美的大棕蝠中分离并鉴定了一种γ疱疹病毒（Eptesicus fuscus 疱疹病毒，EfHV）。由于已知疱疹病毒会从潜伏感染中重新激活，以响应各种压力源，因此 EfHV 为我们提供了一个机会来研究生理、行为或环境变化如何影响大棕蝠与 EfHV 的关系。为了了解病毒的生物学特性以及这些蝙蝠在冬眠期间经历的长时间蛰伏期以及唤醒时的压力如何影响病毒-宿主关系，我们试图在野生捕获的非冬眠蝙蝠以及从冬眠中苏醒的圈养蝙蝠的血液中检测到该病毒。我们比较了 EfHV 在圈养冬眠蝙蝠（使用 PCR）和野生捕获的非冬眠蝙蝠（使用 ELISA）血液中的流行率。我们仅在圈养冬眠蝙蝠的血液中检测到 EfHV（27.8%=10/36），而在野生捕获的非冬眠蝙蝠的血液中未检测到 EfHV（0.0%=0/43）。相比之下，非冬眠蝙蝠的 EfHV 特异性抗体滴度高于冬眠蝙蝠。我们的研究表明：（a）血液中的病毒 DNA 表明从潜伏中重新激活，（b）长时间的冬眠导致免疫力下降，（c）从冬眠中唤醒的压力会在抗病毒免疫力较低的蝙蝠中重新激活病毒（由体液免疫反应表明），以及（d）在病毒重新激活后，非冬眠蝙蝠的抗病毒免疫力增加。
