Pearce Melissa B, Pappas Claudia, Gustin Kortney M, Davis C Todd, Pantin-Jackwood Mary J, Swayne David E, Maines Taronna R, Belser Jessica A, Tumpey Terrence M
Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia.
Southeast Poultry Research Laboratory, Agricultural Research Service, US Department of Agriculture, Athens, Georgia.
Virology. 2017 Feb;502:114-122. doi: 10.1016/j.virol.2016.12.024. Epub 2016 Dec 27.
Sporadic avian to human transmission of highly pathogenic avian influenza (HPAI) A(H5N1) viruses necessitates the analysis of currently circulating and evolving clades to assess their potential risk. Following the spread and sustained circulation of clade 2 viruses across multiple continents, numerous subclades and genotypes have been described. To better understand the pathogenesis associated with the continued diversification of clade 2A(H5N1) influenza viruses, we investigated the relative virulence of eleven human and poultry isolates collected from 2006 to 2013 by determining their ability to cause disease in the ferret model. Numerous clade 2 viruses, including a clade 2.2 avian isolate, a 2.2.2.1 human isolate, and two 2.2.1 human isolates, were found to be of low virulence in the ferret model, though lethality was detected following infection with one 2.2.1 human isolate. In contrast, three of six clade 2.3.2.1 avian isolates tested led to severe disease and death among infected ferrets. Clade 2.3.2.1b and 2.3.2.1c isolates, but not 2.3.2.1a isolates, were associated with ferret lethality. All A(H5N1) viruses replicated efficiently in the respiratory tract of ferrets regardless of their virulence and lethality. However, lethal isolates were characterized by systemic viral dissemination, including detection in the brain and enhanced histopathology in lung tissues. The finding of disparate virulence phenotypes between clade 2A(H5N1) viruses, notably differences between subclades of 2.3.2.1 viruses, suggests there are distinct molecular determinants present within the established subclades, the identification of which will assist in molecular-based surveillance and public health efforts against A(H5N1) viruses.
高致病性禽流感(HPAI)A(H5N1)病毒从禽类向人类的散发性传播,使得有必要对当前正在传播和不断演变的进化枝进行分析,以评估其潜在风险。在2.2进化枝病毒在多个大陆传播并持续流行之后,已描述了众多亚进化枝和基因型。为了更好地了解与2.2进化枝A(H5N1)流感病毒持续多样化相关的发病机制,我们通过测定2006年至2013年收集的11株人类和禽类分离株在雪貂模型中引发疾病的能力,研究了它们的相对毒力。发现众多2.2进化枝病毒,包括一株2.2.2禽类分离株、一株2.2.2.1人类分离株和两株2.2.1人类分离株,在雪貂模型中毒力较低,不过在感染一株2.2.1人类分离株后检测到了致死情况。相比之下,所检测的6株2.3.2.1禽类分离株中有3株在感染的雪貂中导致了严重疾病和死亡。2.3.2.1b和2.3.2.1c分离株而非2.3.2.1a分离株与雪貂致死有关。所有A(H5N1)病毒无论其毒力和致死性如何,均能在雪貂的呼吸道中高效复制。然而,致死性分离株的特征是病毒在全身扩散,包括在脑中被检测到以及肺组织中组织病理学变化增强。2.2进化枝A(H5N1)病毒之间存在不同毒力表型的发现,尤其是2.3.2.1病毒亚进化枝之间的差异,表明在已确定的亚进化枝中存在不同的分子决定因素,对其进行鉴定将有助于针对A(H5N1)病毒开展基于分子的监测和公共卫生工作。