Mettenleiter T C, Lomniczi B, Sugg N, Schreurs C, Ben-Porat T
Department of Microbiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
J Virol. 1988 Jan;62(1):12-9. doi: 10.1128/JVI.62.1.12-19.1988.
Several attenuated strains of pseudorabies virus contain genomes that carry a deletion in their short unique (Us) component. The sizes of the deletions are different in the various attenuated strains; the deletions may include part of one of the inverted repeats as well as part of the Us region of the genome. In most cases, the deletion includes the gene encoding the glycoprotein gI. The attenuated strains with a deletion in their S component have a common history of having been cultivated in chicken embryo fibroblasts (CEF). We show here that passage of wild-type virus in CEF promotes the emergence of populations of virions with a deletion in their S component. The emergence of these mutants is the result of their growth advantage over the wild type and is related to the lack of expression of gI, as shown by the following. (i) The Norden strain (which has a deletion in the Us) was marker rescued to restore an intact Us. The nonrescued Norden strain had a growth advantage over the rescued Norden strain in CEF. (ii) Passage of wild-type (gI+) virus in CEF but not in rabbit kidney or pig kidney cells resulted invariably in the emergence of virions whose genomes had a deletion in the S component. (iii) Passage of a gI- mutant in CEF did not result in the emergence of such virions. The emergence of virions with a deletion in their S component thus appears to be linked to gI expression. We conclude that gI is deleterious to the growth of pseudorabies virus in CEF and that this effect is cell type specific.
几种伪狂犬病病毒减毒株的基因组在其短独特（Us）组分中存在缺失。不同减毒株的缺失大小不同；这些缺失可能包括一个反向重复序列的一部分以及基因组Us区域的一部分。在大多数情况下，缺失包括编码糖蛋白gI的基因。其S组分存在缺失的减毒株有一个共同的历史，即都在鸡胚成纤维细胞（CEF）中培养过。我们在此表明，野生型病毒在CEF中传代促进了S组分存在缺失的病毒粒子群体的出现。这些突变体的出现是由于它们相对于野生型具有生长优势，并且如以下所示与gI表达缺失有关。（i）诺登毒株（其Us存在缺失）经标记拯救以恢复完整的Us。未拯救的诺登毒株在CEF中比拯救后的诺登毒株具有生长优势。（ii）野生型（gI +）病毒在CEF中传代，但在兔肾或猪肾细胞中传代则不会导致基因组S组分存在缺失的病毒粒子出现。（iii）gI - 突变体在CEF中传代不会导致此类病毒粒子出现。因此，S组分存在缺失的病毒粒子的出现似乎与gI表达有关。我们得出结论，gI对伪狂犬病病毒在CEF中的生长有害，并且这种效应具有细胞类型特异性。
