Beard C W, Spindler K R
Department of Genetics, University of Georgia, Athens 30602, USA.
J Virol. 1996 Sep;70(9):5867-74. doi: 10.1128/JVI.70.9.5867-5874.1996.
Early region 3 (E3) of mouse adenovirus type 1 has the potential to produce three proteins which have identical amino termini but unique carboxy-terminal sequences. Three recombinant deletion viruses were constructed so that each could produce only one of the three E3 proteins. A fourth mutant that should produce no E3 proteins was also constructed. These recombinants were able to grow in mouse 3T6 cells and produced wild-type levels of viral mRNAs and proteins except for those specifically deleted by the mutations. Early mRNA production from the mutant viruses was analyzed by reverse transcriptase PCR and confirmed that each deletion mutant would be able to produce only one of the three E3 proteins. Late mRNA production was analyzed by Northern (RNA) blotting and found to be similar in wild-type and mutant viruses. Capsid morphology was unaltered in the mutant viruses as seen by electron microscopy. Immunoprecipitation of E3 proteins from infections of mouse 3T6 cells using an antiserum specific for all three E3 proteins was used to examine the effect of the introduced mutations on protein expression. Two mutants produced only one class of E3 protein as predicted from their specific mutations and mRNA expression profiles. One mutant virus failed to produce any detectable E3 proteins. The predicted E3-null mutant was found to be leaky and could produce low levels of E3 proteins. Outbred Swiss mice were infected with the E3 mutant viruses to determine if the E3 proteins have an effect on the pathogenicity of the virus in mice. All of the mutants showed decreased pathogenicity as determined by increased 50% lethal doses, indicating that the proteins of the E3 region are important determinants of the pathogenesis of mouse adenovirus in its natural host.
1型小鼠腺病毒的早期区域3(E3)有潜力产生三种蛋白质,它们具有相同的氨基末端,但羧基末端序列独特。构建了三种重组缺失病毒,使得每种病毒只能产生三种E3蛋白中的一种。还构建了第四种预计不产生E3蛋白的突变体。这些重组体能够在小鼠3T6细胞中生长,并产生野生型水平的病毒mRNA和蛋白质,但那些被突变特异性删除的除外。通过逆转录酶PCR分析突变病毒的早期mRNA产生情况,证实每个缺失突变体只能产生三种E3蛋白中的一种。通过Northern(RNA)印迹分析晚期mRNA产生情况,发现野生型和突变病毒相似。电子显微镜观察发现突变病毒的衣壳形态未改变。使用对所有三种E3蛋白特异的抗血清,从小鼠3T6细胞感染中免疫沉淀E3蛋白,以检查引入的突变对蛋白质表达的影响。两个突变体如根据其特定突变和mRNA表达谱所预测的那样,只产生一类E3蛋白。一个突变病毒未能产生任何可检测到的E3蛋白。发现预计的E3缺失突变体有渗漏现象,能够产生低水平的E3蛋白。用E3突变病毒感染远交系瑞士小鼠,以确定E3蛋白是否对病毒在小鼠中的致病性有影响。如通过增加的50%致死剂量所确定的,所有突变体的致病性均降低,表明E3区域的蛋白质是小鼠腺病毒在其自然宿主中发病机制的重要决定因素。