B组柯萨奇病毒致糖尿病表型与复制效率相关。
Group B coxsackievirus diabetogenic phenotype correlates with replication efficiency.
作者信息
Kanno Toru, Kim Kisoon, Kono Ken, Drescher Kristen M, Chapman Nora M, Tracy Steven
机构信息
Enterovirus Research Laboratory, Department of Pathology and Microbiology, University of Nebraska Medical Center, 986495 Nebraska Medical Center, Omaha, NE 68198-6495, USA.
出版信息
J Virol. 2006 Jun;80(11):5637-43. doi: 10.1128/JVI.02361-05.
Abstract
Group B coxsackieviruses can initiate rapid onset type 1 diabetes (T1D) in old nonobese diabetic (NOD) mice. Inoculating high doses of poorly pathogenic CVB3/GA per mouse initiated rapid onset T1D. Viral protein was detectable in islets shortly after inoculation in association with beta cells as well as other primary islet cell types. The virulent strain CVB3/28 replicated to higher titers more rapidly than CVB3/GA in the pancreas and in established beta cell cultures. Exchange of 5'-nontranslated regions between the two CVB3 strains demonstrated a variable impact on replication in beta cell cultures and suppression of in vivo replication for both strains. While any CVB strain may be able to induce T1D in prediabetic NOD mice, T1D onset is linked both to the viral replication rate and infectious dose.
摘要
B组柯萨奇病毒可在老年非肥胖糖尿病（NOD）小鼠中引发快速发病的1型糖尿病（T1D）。每只小鼠接种高剂量致病性较弱的CVB3/GA可引发快速发病的T1D。接种后不久，在胰岛中可检测到病毒蛋白，其与β细胞以及其他主要胰岛细胞类型相关。在胰腺和已建立的β细胞培养物中，强毒株CVB3/28比CVB3/GA更快地复制到更高滴度。两种CVB3毒株之间5'非翻译区的交换对β细胞培养物中的复制以及两种毒株的体内复制抑制都有不同影响。虽然任何CVB毒株都可能能够在糖尿病前期NOD小鼠中诱导T1D，但T1D的发病与病毒复制率和感染剂量都有关联。
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