Broom A K, Lindsay M D, Johansen C A, Wright A E, Mackenzie J S
Department of Microbiology, University of Western Australia, Queen Elizabeth II Medical Centre, Nedlands.
Am J Trop Med Hyg. 1995 Jul;53(1):95-9.
Two possible mechanisms are described for the initiation of Murray Valley encephalitis (MVE) virus activity in arid, epizootic regions of tropical Australia. Virus isolations were made from mosquitoes trapped shortly after the first heavy wet season rains and flooding in the east Kimberley, which followed approximately nine months of drought. A number of isolates of MVE virus were obtained, including isolates from pools of blood-engorged Culex annulirostris mosquitoes and from a single pool of male Aedes tremulus mosquitoes. The results strongly suggested that MVE virus activity was due both to its introduction in viremic vertebrate hosts, from which first-generation mosquitoes became infected following blood meals, and also to reactivation of vertically transmitted virus from desiccation-resistant eggs of Ae. tremulus. Both mechanisms are discussed with respect to environmental conditions.
文中描述了澳大利亚热带干旱地区引发墨累谷脑炎（MVE）病毒活动的两种可能机制。在东金伯利地区经历了约九个月干旱后，首次出现强降雨和洪水后的短时间内，从捕获的蚊子中分离出了病毒。获得了多个MVE病毒分离株，包括从吸食饱血的环纹库蚊群体以及单个雄性颤抖伊蚊群体中分离出的毒株。结果有力地表明，MVE病毒活动既是由于其在病毒血症脊椎动物宿主中的引入，第一代蚊子在吸食血液后从中感染，也是由于从颤抖伊蚊耐干燥卵中垂直传播的病毒重新激活。针对环境条件对这两种机制都进行了讨论。
