DEFECTIVE-INTERFERING PARTICLES OF THE HUMAN PARVOVIRUS ADENO-ASSOCIATED VIRUS
DEFECTIVE-INTERFERING PARTICLES OF THE HUMAN PARVOVIRUS ADENO-ASSOCIATED VIRUS
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DOI：
10.1016/0042-6822(79)90446-x
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发表时间：
1979-01-01
期刊：
影响因子：
3.7
通讯作者：
CARTER, BJ
中科院分区：
文献类型：
--
作者：
LAUGHLIN, CA;MYERS, MW;CARTER, BJ
以前的研究表明，腺相关病毒（AAV）与辅助腺病毒一起在人口腔癌KB细胞中生长，产生了几种由其在CsCl中的浮力密度定义的颗粒。主要密度类别分别称为AAV（1.45）、AAV（1.41）、AAV（1.35）和AAV（1.32），其中颗粒密度写在括号中。含有标准基因组的AAV（1.45）和AAV（1.41）颗粒是仅有的感染性AAV颗粒。这些感染性AAV颗粒表现出自身干扰。光密度AAV（1.35）和（1.32）颗粒含有异常（缺失和/或sanp-back）基因组。报道的实验表明，低密度AAV颗粒无感染性，但干扰AAV的复制（1.41）。干扰是细胞内的，并导致抑制标准（14.5 S）AAV基因组的合成。在某些情况下，异常的较短的AAV DNA的合成也伴随增加。光密度颗粒的抑制活性被UV照射消除。轻AAV颗粒群含有DI颗粒。观察到的AAV（1.45）或AAV（1.41）病毒的自身干扰假定是由于AAV DI颗粒。AAV DI基因组的复制似乎需要复制的标准AAV基因组的存在。这被解释为意指AAV的子代链复制需要AAV特异性产物，推测为AAV衣壳蛋白。与标准的感染性AAV相反，单独的AAV DI颗粒不抑制辅助腺病毒的复制。
It was previously shown that adeno-associated virus (AAV) grown in [human oral carcinoma] KB cells with a helper adenovirus, produced several classes of particles defined by their buoyant density in CsCl. The predominant density classes were referred to as AAV(1.45), AAV(1.41), AAV(1.35) and AAV(1.32), respectively, where the density of the particle was written in the parentheses. The AAV(1.45) and AAV(1.41) particles which contained standard genomes were the only infectious AAV particles. These infectious AAV particles exhibited autointerference. The light-density AAV(1.35) and (1.32) particles contained aberrant (deleted and/or sanp-back) genomes. Experiments are reported which show that the light-density AAV particles were noninfectious but interfered with the replication of AAV(1.41). The interference was intracellular and resulted in inhibition of synthesis of standard (14.5 S) AAV genomes. In some cases there was also a concomitant increase in synthesis of aberrant, shorter AAV DNA. The inhibitory activity of the light-density particles was abolished by UV irradiation. The population of light AAV particles contained DI particles. The observed autointerference of AAV(1.45) or AAV(1.41) virus is postulated to be due to AAV DI particles. Replication of AAV DI genomes appeared to require the presence of replicating, standard AAV genomes. This is interpreted to mean that progeny strand replication of AAV requires an AAV-specified product, presumably the AAV capsid protein. In contrast to standard, infectious AAV, the AAV DI particles alone do not inhibit replication of the helper adenovirus.