Inhibition of Sendai virus genome replication due to promoter-increased selectivity: a possible role for the accessory C proteins

被引:77
作者
Tapparel, C [1 ]
Hausmann, S [1 ]
Pelet, T [1 ]
Curran, J [1 ]
Kolakofsky, D [1 ]
Roux, L [1 ]
机构
[1] UNIV GENEVA, SCH MED, CMU, DEPT GENET & MICROBIOL, CH-1211 GENEVA 4, SWITZERLAND
关键词
D O I
10.1128/JVI.71.12.9588-9599.1997
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The role of the negative-stranded virus accessory C proteins is difficult to assess because they appear sometimes as nonessential and thereby of no function. On the other hand, when a function is found, as in the case of Sendai virus, it represents an enigma, in that the C proteins inhibit replication under conditions where the infection follows an exponential course. Furthermore, this inhibitory function is exerted differentially: in contrast to the replication of internal deletion defective interfering (DI) RNAs, that of copy-back DI RNAs appears to escape inhibition, under certain experimental conditions (in vivo assay). In a reexamination of the C effect by the reverse genetics approach, it was found that copy-back RNA replication is inhibited by C in vivo as well, under conditions where the ratio of C to copy-back template is increased, This effect can be reversed by an increase in P but not L protein. The ''rule of six'' was differentially observed in the presence or absence of C. Finally, a difference in the ability of the replicating complex to tolerate promoter modifications in RNA synthesis initiation was shown to occur in the presence or the absence of C as well, We propose that C acts by increasing the selectivity of the replicating complex for the promoter cis-acting elements governing its activity. The inhibitory effect of C becomes the price to pay for this increased selectivity.
引用
收藏
页码:9588 / 9599
页数:12
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