Semliki forest virus persistence in mouse L929 cells.
Semliki forest virus persistence in mouse L929 cells.
复制标题
Semliki 森林病毒在小鼠 L929 细胞中持续存在。
DOI：
10.1016/0042-6822(80)90560-7
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发表时间：
1980
期刊：
影响因子：
3.7
通讯作者：
S.I.T. Kennedy
中科院分区：
文献类型：
--
作者：
Judy Meinkoth;S.I.T. Kennedy
我们提出了一种利用甲型病毒类森林病毒(SFV)建立和维持小鼠L929细胞持续感染的特征。如果不对L细胞进行干扰素预处理，只有使用富含缺陷干扰(DI)颗粒的接种物才能建立持续感染。一种这种持续感染的培养物(载体培养)现在已有一年多的历史，其特征是细胞(I)通常在形态上与未感染的细胞相同，(Ii)释放不同滴度的传染性病毒，(Iii)周期性地进入危象状态，在此期间许多细胞死亡，以及(Iv)可通过病毒抗血清治疗治愈病毒。在第一次危象后，在载体培养中任何时候都无法检测到DI颗粒。持续感染的细胞中只有一小部分(0.1-4.5%)释放了感染性病毒，病毒结构抗原阳性的细胞只有1-20%。持续感染的细胞对同源病毒和异源病毒的重叠感染都具有抵抗力。干扰素在载体培养的液体中以不同的数量存在。事实上，通过用100个单位/毫升的小鼠干扰素对未感染细胞进行预处理，可以很容易地建立类似的持续感染。在这种情况下，接种液中不需要DI颗粒。利用寡核苷酸指纹图谱，我们证明了病毒基因组突变发生在持续期间，其中许多突变发生在编码病毒结构蛋白的基因中。在这些观察的基础上，我们提出了SFV在小鼠L929细胞中持续存在的模型。
We present a characterization of the establishment and maintenance of a persistent infection of mouse L929 cells using the alphavirus Semlike Forest virus (SFV). Without interferon pretreatment of the L cells, a persistent infection could only be established using an inoculum rich in defective-interfering (DI) particles. One such persistently infected culture (carrier culture) now over 1 year old, is characterized by cells (i) which are usually morphologically identical to uninfected cells, (ii) which release variable titers of infectious virus, (iii) which periodically enter a state of crisis during which many of the cells perish, and (iv) which can be cured of virus by treatment with viral antiserum. After the first crisis, DI particles could not be detected at any time in the carrier culture. Only a small proportion (0.1–4.5%) of the persistently infected cells released infectious virus and only 1–20% were positive for viral structural antigen. The persistently infected cells were resistant to superinfection by both homologous and heterologous virus. Interferon was present in variable quantities in the fluid from the carrier culture. Indeed a similar persistent infection could readily be established by pretreatment of uninfected cells with 100 units/ml of mouse interferon. In this case DI particles were not required in the inoculum. Using oligonucleotide fingerprinting we demonstrate that viral genomic mutations occur during persistence and that many of these mutations occur in genes coding for the virus structural proteins. On the basis of these observations we present a model for SFV persistence in mouse L929 cells.