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对感染不同 multiplicity(感染复数,MOI)的 2 型单纯疱疹病毒(HSV - 2)的 CV - 1 细胞培养物中 DNA 合成动力学的研究。

Studies on kinetics of DNA synthesis in CV-1 cell cultures infected with different multiplicities (MOI) of Herpes simplex virus type 2 (HSV-2).

作者信息

Dostal V, Kroath H, Binder M

出版信息

Osterr Z Onkol. 1976 May;3(1-2):3-8.

PMID:186742
Abstract

Infection of CV-1 cell cultures with HSV-2 at MOI 5 respectively 1PFU/cell resulted in markedly different patterns of DNA-synthesis. Isolation and separation of cellular and viral DNA on CsCl equilibrium density gradients during the "late" phase after infection with 5PFU/cell revealed a rapid increase in synthesis of virus-specific DNA (which banded at density q25 = 1.729 g/ccm) while synthesis of host cell DNA (banding at 1.705 g/ccm) was constantly inhibited. 15 hours after infection and incubation with labelled medium, around infection and incubation with labelled medium, around 75% of total isolated DNA was virus-specific. On lowering the MOI to 1 PFU/cell, however, synthesis of host cell DNA continued and was even partially stimulated during the late phase whereas synthesis of virus-specific DNA advanced only slowly. 16 hours after infection, approximately 25% of the total assayed after infection, approximately 25% of the total assayed DNA was virus-specific and the amount of host cell DNA approached values of uninfected control cells. 24 hours after infection and incubation, virus specific DNA rose to approximately 45% of overall DNA assayed, and synthesis of host cell DNA was completely inhibited. However, infectivity rose constantly and reached 106.8 TCD 50/ml at 22 hours p.i. These findings were independent of passage number of CV-cell culture, and there were no alterations in karyotype and morphological behaviour of the cells.

摘要

以5个感染复数(MOI)即每细胞1个空斑形成单位(PFU)的HSV - 2感染CV - 1细胞培养物,导致DNA合成模式明显不同。在用每细胞5个PFU感染后的“晚期”,通过氯化铯平衡密度梯度对细胞和病毒DNA进行分离,结果显示病毒特异性DNA(密度为q25 = 1.729 g/ccm处形成条带)的合成迅速增加,而宿主细胞DNA(密度为1.705 g/ccm处形成条带)的合成持续受到抑制。在感染并与标记培养基孵育15小时后,即感染并与标记培养基孵育前后,分离得到的总DNA中约75%是病毒特异性的。然而,当将MOI降至每细胞1个PFU时,宿主细胞DNA的合成在晚期仍继续,甚至部分受到刺激,而病毒特异性DNA的合成进展缓慢。感染16小时后,感染后检测的总DNA中约25%是病毒特异性的,宿主细胞DNA的量接近未感染对照细胞的值。感染并孵育24小时后,病毒特异性DNA升至检测的总DNA的约45%,宿主细胞DNA的合成被完全抑制。然而,感染性持续上升,在感染后22小时达到106.8半数组织培养感染剂量(TCD50)/毫升。这些发现与CV - 1细胞培养物的传代次数无关,并且细胞的核型和形态行为没有改变。

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