Silverman L, Anderson K P, Klessig D F
J Virol. 1985 Dec;56(3):814-20. doi: 10.1128/JVI.56.3.814-820.1985.
In abortive infections of monkey cells by Ad2+ND5, the synthesis of the simian virus 40-specific 42,000-molecular-weight (42K) protein was reduced approximately 10-fold compared with a productive coinfection by Ad2+ND5 plus Ad2hr400 and about 20-fold compared with productive infections by Ad2+ND5 plus simian virus 40 or by Ad2+ND2 alone. However, the level of Ad2+ND5-specific mRNA was depressed twofold or less in abortive infections compared with productive infections. Moreover, the 42K mRNA isolated from abortive Ad2+ND5 infections translated in vitro with the same efficiency as the mRNA isolated from productive coinfections. This is analogous to the block to synthesis of the adenovirus fiber polypeptide in monkey cells (Anderson and Klessig, J. Mol. Appl. Genet. 2:31-43, 1983). Also like fiber protein, the increased level of the 42K protein found in productive infections was due to enhanced synthesis, not increased stability of the protein. Our results suggest that the synthesis of the Ad2+ND5-specified 42K protein and the adenovirus fiber protein are regulated in similar posttranscriptional manners.
在猴细胞被Ad2+ND5进行流产感染时，与Ad2+ND5加Ad2hr400进行的有效共感染相比，猿猴病毒40特异性的42,000分子量（42K）蛋白质的合成减少了约10倍；与Ad2+ND5加猿猴病毒40进行的有效感染或单独的Ad2+ND2进行的有效感染相比，减少了约20倍。然而，与有效感染相比，在流产感染中Ad2+ND5特异性mRNA的水平降低了两倍或更少。此外，从流产的Ad2+ND5感染中分离出的42K mRNA在体外翻译的效率与从有效共感染中分离出的mRNA相同。这类似于猴细胞中腺病毒纤维多肽合成的阻断（Anderson和Klessig，《分子应用遗传学杂志》2:31-43，1983）。同样与纤维蛋白一样，在有效感染中发现的42K蛋白质水平的增加是由于合成增强，而不是蛋白质稳定性的增加。我们的结果表明，Ad2+ND5指定的42K蛋白质和腺病毒纤维蛋白的合成以类似的转录后方式受到调控。
