Chromosomal Integration by Human Herpesviruses 6A and 6B
Chromosomal Integration by Human Herpesviruses 6A and 6B
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DOI：
10.1007/978-981-10-7230-7_10
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发表时间：
2018-01-01
期刊：
影响因子：
--
通讯作者：
Flamand, Louis
中科院分区：
文献类型：
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作者：
Flamand, Louis
在感染后，根据感染的细胞类型，人疱疹病毒6A（HHV-6A）和6 B（HHV-6 B）可以复制或进入潜伏状态。HHV-6A和HHV-6 B可以将它们的基因组整合到宿主染色体中，作为建立潜伏期的一种方式。病毒整合发生在染色体亚端粒/端粒连接处附近。当HHV-6感染和整合发生在配子中时，病毒可以通过遗传传播。遗传染色体整合的HHV-6（iciHHV-6）阳性个体每个体细胞携带一个整合的HHV-6拷贝。根据采样的地理区域，iciHHV-6（+）个体的患病率在0.6%至2%之间变化。本章讨论了导致病毒整合和从潜伏期重新激活的机制，以及与iciHHV-6相关的一些生物学和医学后果。
Upon infection and depending on the infected cell type, human herpesvirus 6A (HHV-6A) and 6B (HHV-6B) can replicate or enter a state of latency. HHV-6A and HHV-6B can integrate their genomes into host chromosomes as one way to establish latency. Viral integration takes place near the subtelomeric/telomeric junction of chromosomes. When HHV-6 infection and integration occur in gametes, the virus can be genetically transmitted. Inherited chromosomally integrated HHV-6 (iciHHV-6)-positive individuals carry one integrated HHV-6 copy per somatic cell. The prevalence of iciHHV-6(+) individuals varies between 0.6% and 2%, depending on the geographical region sampled. In this chapter, the mechanisms leading to viral integration and reactivation from latency, as well as some of the biological and medical consequences associated with iciHHV-6, were discussed.