Weaver Scott C
Institute for Human Infections and Immunity and Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA
mBio. 2017 Jan 10;8(1):e02063-16. doi: 10.1128/mBio.02063-16.
The mechanisms responsible for the dramatic emergence of Zika virus (ZIKV), accompanied by congenital Zika syndrome and Guillain-Barré syndrome (GBS), remain unclear. However, two hypotheses are prominent: (i) evolution for enhanced urban transmission via adaptation to mosquito vectors, or for enhanced human infection to increase amplification, or (ii) the stochastic introduction of ZIKV into large, naive human populations in regions with abundant Aedes aegypti populations, leading to enough rare, severe infection outcomes for their first recognition. Advances in animal models for human infection combined with improvements in serodiagnostics, better surveillance, and reverse genetic approaches should provide more conclusive evidence of whether mosquito transmission or human pathogenesis changed coincidentally with emergence in the South Pacific and the Americas. Ultimately, understanding the mechanisms of epidemic ZIKV emergence, and its associated syndromes, is critical to predict future risks as well as to target surveillance and control measures in key locations.
导致寨卡病毒(ZIKV)急剧出现并伴有先天性寨卡综合征和吉兰 - 巴雷综合征(GBS)的机制仍不清楚。然而,有两种假设较为突出:(i)通过适应蚊媒实现增强的城市传播进化,或增强人类感染以增加病毒扩增,或者(ii)寨卡病毒随机引入埃及伊蚊数量丰富地区的大量未接触过该病毒的人群中,导致首次发现足够多的罕见严重感染病例。人类感染动物模型的进展,结合血清诊断学的改进、更好的监测以及反向遗传学方法,应能提供更确凿的证据,证明在南太平洋和美洲出现疫情时,蚊媒传播或人类发病机制是否同时发生了变化。最终,了解寨卡病毒流行的出现机制及其相关综合征,对于预测未来风险以及在关键地点确定监测和控制措施至关重要。