Spence S L, Tack L C, Wright J H, Carswell S, Pipas J M
Department of Biological Sciences, University of Pittsburgh, Pennsylvania 15260.
In Vitro Cell Dev Biol. 1990 Jun;26(6):604-11. doi: 10.1007/BF02624210.
SV40 viruses bearing mutations at the carboxy-terminus of large T antigen exhibit a host-range phenotype: such viruses are able to grow in BSC monkey kidney cells at 37 degrees C, but give at least 10,000-fold lower yields than wild type virus in BSC cells at 32 degrees C or in CV1 monkey kidney cells at either temperature. The block to infection in the nonpermissive cell type occurs after the onset of viral DNA replication. Infectious progeny virions are produced at very low efficiency. Although capsid proteins are synthesized at decreased levels, this does not account for the magnitude of the defect. Presumably some step of virion assembly or maturation is affected in these mutants. We have previously reported that the viral agnogene product, a protein thought to be involved in viral assembly or release, fails to accumulate in CV1 cells infected with host-range mutants. In polyoma virus the middle T antigen plays a role in virion maturation by influencing the phosphorylation of capsid proteins. In this communication we show that host-range mutants fail to undergo productive infection of CV1 cells expressing middle T antigen. These mutants do form plaques on an agnoprotein-expressing cell line. However, the agnoprotein does not seem to act by correcting the mutational block but rather increases the efficiency of plaque formation.
在大T抗原羧基末端携带突变的SV40病毒表现出宿主范围表型：此类病毒能够在37摄氏度下在BSC猴肾细胞中生长，但在32摄氏度下的BSC细胞中或在任一温度下的CV1猴肾细胞中，其产量比野生型病毒低至少10000倍。在非允许细胞类型中，感染阻断发生在病毒DNA复制开始之后。有感染性的子代病毒颗粒产生效率非常低。虽然衣壳蛋白的合成水平降低，但这并不能解释缺陷的程度。推测这些突变体中病毒粒子组装或成熟的某些步骤受到了影响。我们之前报道过，病毒agnogene产物（一种被认为参与病毒组装或释放的蛋白质）在感染宿主范围突变体的CV1细胞中无法积累。在多瘤病毒中，中T抗原通过影响衣壳蛋白的磷酸化在病毒粒子成熟中发挥作用。在本通讯中，我们表明宿主范围突变体无法对表达中T抗原的CV1细胞进行有效感染。这些突变体确实能在表达agnoprotein的细胞系上形成噬斑。然而，agnoprotein似乎并不是通过纠正突变阻断来起作用，而是提高了噬斑形成的效率。
