Yura Y, Terashima K, Iga H, Yanagawa T, Yoshida H, Hayashi Y, Sato M
Arch Virol. 1986;90(3-4):249-60. doi: 10.1007/BF01317374.
Human neuroblastoma (IMR-32) cells were infected with herpes simplex virus type 2 (HSV-2) at a multiplicity of infection (MOI) of 2 plaque-forming units (PFU)/cell and were cultured at 40 degrees C for 14 days. Then neither infectious virus particles nor virus capsids were detected in these cells whereas the presence of virus-specific antigens was observed by immunofluorescent antibody staining technique in 16.9 +/- 3.2 per cent of the infected cell population. When the cultivation temperature was shifted down from 40 degrees C to 35 degrees C, reactivation of virus growth occurred after lag periods of 2-9 days. These findings indicate that the IMR-32 cells can be latently infected with HSV-2 at 40 degrees C and that virus growth may be inhibited at the level of synthesis of virus-specific macromolecules or at some step preceding nucleocapsid formation.
人神经母细胞瘤（IMR - 32）细胞以每细胞2个空斑形成单位（PFU）的感染复数（MOI）感染单纯疱疹病毒2型（HSV - 2），并在40℃培养14天。之后在这些细胞中既未检测到感染性病毒颗粒，也未检测到病毒衣壳，而通过免疫荧光抗体染色技术在16.9±3.2%的感染细胞群体中观察到了病毒特异性抗原的存在。当培养温度从40℃降至35℃时，在2 - 9天的延迟期后病毒生长重新激活。这些发现表明，IMR - 32细胞在40℃时可被HSV - 2潜伏感染，并且病毒生长可能在病毒特异性大分子合成水平或核衣壳形成之前的某个步骤受到抑制。
