Kosz-Vnenchak M, Coen D M, Knipe D M
Department of Microbiology, Harvard Medical School, Boston, Massachusetts 02115.
J Virol. 1990 Nov;64(11):5396-402. doi: 10.1128/JVI.64.11.5396-5402.1990.
Infection of cells by herpes simplex virus (HSV) can lead to either lytic, productive infection or nonlytic, latent infection. The factors influencing this infection pathway decision are largely unknown. Thymidine kinase-negative mutant viruses can establish latent infection in neurons of mouse trigeminal ganglia but do not replicate productively in these cells. We show that during the early stages of establishment of latency by these mutants, expression of viral lytic genes is drastically reduced or undetectable as assayed by in situ hybridization. Thus, establishment of latent infection by HSV can occur despite severely restricted levels of lytic gene expression. This suggests that the block to productive replication during establishment of latent infection by HSV occurs before or early during the expression of alpha genes.
单纯疱疹病毒（HSV）感染细胞可导致溶解性、增殖性感染或非溶解性潜伏感染。影响这种感染途径选择的因素大多未知。胸苷激酶阴性突变病毒可在小鼠三叉神经节神经元中建立潜伏感染，但在这些细胞中不能进行增殖性复制。我们发现，在这些突变体建立潜伏感染的早期阶段，通过原位杂交检测，病毒溶解性基因的表达大幅降低或无法检测到。因此，尽管溶解性基因表达水平受到严重限制，HSV仍可建立潜伏感染。这表明，HSV在建立潜伏感染期间对增殖性复制的阻断发生在α基因表达之前或早期。
