5' terminal deletions in the genome of a coxsackievirus B2 strain occurred naturally in human heart
5' terminal deletions in the genome of a coxsackievirus B2 strain occurred naturally in human heart
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DOI：
10.1016/j.virol.2008.02.030
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发表时间：
2008-06-05
期刊：
影响因子：
3.7
通讯作者：
Tracy, Steven
中科院分区：
文献类型：
--
作者：
Chapman, Nora M.;Kim, Kyung-Soo;Tracy, Steven
肠道病毒可诱导人心肌炎，其可在接种有B组柯萨奇病毒（CVB）的小鼠中建模，并且其中CVB进化为产生缺陷的、末端缺失的基因组。51非翻译区（NTR）是从2002年日本一例肠道病毒相关心肌炎的心脏组织中酶促扩增的。虽然没有检测到完整的51个病毒基因组末端，但51个末端缺失的大小范围为22至36个核苷酸。该病毒基因组的5'三分之一的序列属于现代毒株，与2002年在日本分离的CVB 2毒株密切相关。含有具有22 nt缺失的5' NTR的CVB 3嵌合体在转染HeLa细胞后产生子代病毒。当51 - 22个核苷酸缺失被修复时，病毒诱导小鼠心肌炎，并在小鼠心脏细胞中像野生型病毒一样复制。这是第一次报告这些自然发生的缺陷肠道病毒基因组在人类心肌炎。(c)2008年爱思唯尔公司All rights reserved.
Enteroviruses can induce human myocarditis, which can be modeled in mice inoculated with group B coxsackieviruses (CVB) and in which CVB evolve to produce defective, terminally deleted genomes. The 51 non-translated region (NTR) was enzymatically amplified from heart tissue of a fatal case of enterovirus-associated myocarditis in Japan in 2002. While no intact 51 viral genomic termini were detected, 51 terminal deletions ranged in size from 22 to 36 nucleotides. Sequence of the 5' third of this viral genome is of a modern strain, closely related to CVB2 strains isolated in Japan in 2002. A CVB3 chimera containing the 5' NTR with a 22 nt deletion produced progeny virus upon transfection of HeLa cells. When the 51 22 nucleotide deletion was repaired, the virus induced myrocarditis in mice and replicated like wild type virus in murine heart cells. This is the first report of these naturally-occurring defective enteroviral genomes in human myocarditis. (c) 2008 Elsevier Inc. All rights reserved.