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首页> 外文期刊>Vaccine >Replication and pathogenicity of attenuated human metapneumovirus F mutants in severe combined immunodeficiency mice.
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Replication and pathogenicity of attenuated human metapneumovirus F mutants in severe combined immunodeficiency mice.

机译：减毒的人类偏肺病毒F突变体在严重的联合免疫缺陷小鼠中的复制和致病性。

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This study was to evaluate the replication and pathogenicity of attenuated human metapneumovirus (HMPV) mutants in severe combined immunodeficiency (SCID) mice. SCID mice were intranasally infected with either wild type GFP-rHMPV (WT), or mutant viruses (M1, M2 and M4) with the N-linked glycosylation(s) of the F protein removed. The organs were collected for viral isolation, titration, pulmonary histopathology and mRNA detection by PCR at different time points. WT or mutant viruses were successfully isolated from the lungs of infected mice after inoculation. The titers of WT and M1 peaked on 5th day and remained detectable until 14th day post-inoculation. M2 reached approximately 4 logs lower titer on 5th and 9th day post-inoculation as compared to WT and M1. M4 showed similar growth kinetics to M2. Viral signal was never detected from the heart, liver, spleen, kidney and brain on 5th day post-inoculation. The pulmonary pathology score in the M1 infected mice was similar to WT infected mice but higher than in M2 or M4 infected mice. WT and HMPV mutants can thus only replicate in the lungs of SCID mice. Attenuated M2 and M4 may be considered as candidates for the preparation of vaccine against HMPV.Digital Object Identifier http://dx.doi.org/10.1016/j.vaccine.2011.11.008
机译：这项研究旨在评估在严重的联合免疫缺陷（SCID）小鼠中减毒的人类偏肺病毒（HMPV）突变体的复制和致病性。将SCID小鼠鼻内感染野生型GFP-rHMPV（WT）或突变病毒（M1，M2和M4），并去除F蛋白的N-联糖基化。在不同时间点收集器官用于病毒分离，滴定，肺组织病理学和通过PCR的mRNA检测。接种后，成功地从受感染小鼠的肺中分离出WT或突变病毒。 WT和M1的滴度在第5天达到峰值，直到接种后第14天仍可检测到。与WT和M1相比，M2在接种后第5天和第9天的滴度降低了约4个对数。 M4显示出与M2相似的生长动力学。接种后第5天，从未从心脏，肝脏，脾脏，肾脏和大脑中检测到病毒信号。 M1感染的小鼠的肺病理评分与WT感染的小鼠相似，但高于M2或M4感染的小鼠。因此，WT和HMPV突变体只能在SCID小鼠的肺中复制。减弱的M2和M4可被视为制备针对HMPV的疫苗的候选对象。数字对象标识符http://dx.doi.org/10.1016/j.vaccine.2011.11.008

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