Chen Rubing, Holmes Edward C
Center for Infectious Disease Dynamics, Department of Biology, The Pennsylvania State University, Mueller Laboratory, University Park, PA 16802, USA.
J Mol Evol. 2008 Jun;66(6):655-63. doi: 10.1007/s00239-008-9119-z. Epub 2008 May 27.
Despite their close phylogenetic relationship, type A and B influenza viruses exhibit major epidemiological differences in humans, with the latter both less common and less often associated with severe disease. However, it is unclear what processes determine the evolutionary dynamics of influenza B virus, and how influenza viruses A and B interact at the evolutionary scale. To address these questions we inferred the phylogenetic history of human influenza B virus using complete genome sequences for which the date (day) of isolation was available. By comparing the phylogenetic patterns of all eight viral segments we determined the occurrence of segment reassortment over a 30-year sampling period. An analysis of rates of nucleotide substitution and selection pressures revealed sporadic occurrences of adaptive evolution, most notably in the viral hemagglutinin and compatible with the action of antigenic drift, yet lower rates of overall and nonsynonymous nucleotide substitution compared to influenza A virus. Overall, these results led us to propose a model in which evolutionary changes within and between the antigenically distinct 'Yam88' and 'Vic87' lineages of influenza B virus are the result of changes in herd immunity, with reassortment continuously generating novel genetic variation. Additionally, we suggest that the interaction with influenza A virus may be central in shaping the evolutionary dynamics of influenza B virus, facilitating the shift of dominance between the Vic87 and the Yam88 lineages.
尽管甲型和乙型流感病毒在系统发育上关系密切,但它们在人类中表现出主要的流行病学差异,乙型流感病毒在人类中不太常见,也较少与严重疾病相关。然而,目前尚不清楚哪些过程决定了乙型流感病毒的进化动态,以及甲型和乙型流感病毒在进化尺度上是如何相互作用的。为了解决这些问题,我们利用可获得分离日期(日)的完整基因组序列推断了人类乙型流感病毒的系统发育历史。通过比较所有八个病毒片段的系统发育模式,我们确定了30年采样期内片段重配的发生情况。对核苷酸替代率和选择压力的分析揭示了适应性进化的零星发生,最显著的是在病毒血凝素中,这与抗原漂移的作用相符,但与甲型流感病毒相比,总体和非同义核苷酸替代率较低。总体而言,这些结果使我们提出了一个模型,其中乙型流感病毒抗原性不同的“Yam88”和“Vic87”谱系内部和之间的进化变化是群体免疫变化的结果,并伴有重配不断产生新的遗传变异。此外,我们认为与甲型流感病毒的相互作用可能是塑造乙型流感病毒进化动态的核心因素,促进了Vic87和Yam88谱系之间优势地位的转变。