Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus
Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus
复制标题
DOI：
10.1128/jvi.71.9.6697-6705.1997
复制
发表时间：
1997-09-01
影响因子：
5.4
通讯作者：
Weaver, SC
中科院分区：
文献类型：
--
作者：
Powers, AM;Oberste, MS;Weaver, SC
从20世纪20年代到70年代初，委内瑞拉马脑炎(VEE)疫情和马流行性感冒在美洲周期性地发生，当时假定引起病毒IAB和IC亚型已经灭绝。哥伦比亚和委内瑞拉最近的暴发重新引起了人们对流行病/流行性传染病病毒的来源及其流行病间维持机制的兴趣。我们使用包括E3和E2基因在内的857个核苷酸的逆转录-聚合酶链式反应产物，对VEE病毒分离株进行了系统发育分析，分析范围涵盖了可用的毒株的整个时间和地理范围。分析表明，流行性/流行性传染病病毒与四个不同的地方性亚型ID样谱系密切相关。其中一个谱系出现在哥伦比亚、秘鲁和委内瑞拉，也包括所有流行/流行性分离株；其余三个类似ID的谱系出现在巴拿马、秘鲁、佛罗里达、厄瓜多尔沿海和哥伦比亚西南部，显然与流行性Vee的出现无关。在哥伦比亚/秘鲁/委内瑞拉谱系中，描述了流行/流行性病毒的三个不同的单系群，表明VEE至少独立出现了三次(趋同进化)。比较了具有代表性的、完整的E2氨基酸序列，以确定马的毒力和流行性出现性的潜在决定因素。以前在实验室小鼠衰减过程中涉及的氨基酸在我们检查的自然分离株中通常没有变化，表明它们可能与VEE出现时马的毒力变化无关。大多数信息性氨基酸与系统发育关系相关，而不是表型特征，这表明VEE的出现是由几种不同的突变组合造成的，这些突变产生了具有相似抗原和马毒力表型的病毒。
Venezuelan equine encephalitis (VEE) epidemics and equine epizootics occurred periodically in the Americas from the 1920s until the early 1970s, when the causative viruses, subtypes IAB and IC were postulated to have become extinct. Recent outbreaks in Columbia and Venezuela have renewed interest in the source of epidemic/epizootic viruses and their mechanism of interepizootic maintenance. We performed phylogenetic analyses of VEE virus isolates spanning the entire temporal and geographic range of strains available, using 857-nucleotide reverse transcription-PCR products including the E3 and E2 genes. Analyses indicated that epidemic/epizootic viruses are closely related to four distinct, enzootic subtype ID-like lineages. One of these lineages, which occurs in Columbia, Peru, and Venezuela, also included all of the epidemic/epizootic isolates; the remaining three ID-like lineages, which occur in Panama, Peru, Florida, coastal Ecuador, and southwestern Columbia, were apparently not associated with epizootic VEE emergence. Within the Columbia/Peru/Venezuela lineage, three distinct monophyletic groups of epidemic/epizootic viruses were delineated, indicating that VEE emergence has occurred independently at least three times (convergent evolution). Representative, complete E2 amino acid sequences were compared to identify potential determinants of equine virulence and epizootic emergence. Amino acids implicated previously in laboratory mouse attenuation generally did not vary among the natural isolates that we examined, indicating that they probably are not involved in equine virulence changes associated with VEE emergence. Most informative amino acids correlated with phylogenetic relationships rather than phenotypic characteristics, suggesting that VEE emergence has resulted from several distinct combinations of mutations that generate viruses with similar antigenic and equine virulence phenotype.