Herpesvirus genomes enter the eukaryotic nucleus as large linear double stranded DNA molecules that are free of any proteins (naked DNA). Once inside the nucleus, the HSV-1 genomes immediately associate with proteins that will be instrumental in the organization and regulation of these genomes. These initial interactions are thought to determine the fate of the infecting genomes. In general, the host cell has evolved several mechanisms to suppress viral genomes and induce latent or abortive infections. On the other hand, the virus has evolved to use viral and cellular factors to promote lytic infection. Recent findings suggest that not all viral genomes in the infected nucleus will develop progeny and that not all genetically identical cells will support successful virus propagation. Thus, the decision between different fates of infection is determined at both single-cell and single-genome levels. Here we summarize current knowledge on the conditions and interactions that lead to each outcome and discuss the unknown determinants.

中文翻译：

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进入细胞核的 HSV-1 基因组的命运。

疱疹病毒基因组作为大的线性双链 DNA 分子进入真核细胞核，不含任何蛋白质（裸 DNA）。一旦进入细胞核，HSV-1 基因组立即与有助于组织和调节这些基因组的蛋白质结合。这些最初的相互作用被认为决定了感染基因组的命运。一般来说，宿主细胞已经进化出几种机制来抑制病毒基因组并诱导潜伏或流产感染。另一方面，该病毒已进化为使用病毒和细胞因子来促进溶解感染。最近的研究结果表明，并非所有受感染细胞核中的病毒基因组都会产生后代，并且并非所有基因相同的细胞都会支持病毒的成功繁殖。因此，不同感染命运之间的决定是在单细胞和单基因组水平上决定的。在这里，我们总结了导致每个结果的条件和相互作用的当前知识，并讨论了未知的决定因素。