Bantel-Schaal U, zur Hausen H
Abteilung Virologie, Universität Freiburg, Federal Republic of Germany.
Virology. 1988 May;164(1):64-74. doi: 10.1016/0042-6822(88)90620-4.
Coinfection with HSV-1 and any of the three defective parvoviruses AAV-2, AAV-3, or AAV-5 reduces the HSV-1-induced amplification of SV40 DNA in the SV40-transformed hamster cell lines CO631 and Elona. Moreover, all three viruses significantly decrease HSV-1 replication. The effects are measurable to the same extent in both cell lines and are dependent on the quantity of AAV DNA molecules rather than on infectious AAV particles. It seems unlikely that the inhibitions are due to simple competition but result from complex interactions that involve the terminal sequences of AAV DNA.
单纯疱疹病毒1型(HSV-1)与三种缺陷型细小病毒之一,即腺相关病毒2型(AAV-2)、腺相关病毒3型(AAV-3)或腺相关病毒5型(AAV-5)的共同感染,会降低HSV-1诱导的SV40转化仓鼠细胞系CO631和埃洛纳(Elona)中SV40 DNA的扩增。此外,这三种病毒均显著降低HSV-1的复制。在这两种细胞系中,这些影响在相同程度上是可测量的,并且取决于AAV DNA分子的数量,而不是传染性AAV颗粒的数量。这些抑制作用似乎不太可能是由于简单的竞争,而是由涉及AAV DNA末端序列的复杂相互作用导致的。