IDENTITY OF ATTENUATING LESIONS IN LIVE COLD ADAPTED INFLUENZA VACCINE

我的研究重点一直放在分子机制上 对于冷适应的衰减性和表型 温度敏感性归因于活的、冷适应的(约) 流感A/AA/6/60疫苗。我已经克隆了野生动物的全部八个基因 型(Wt)前体病毒和CAA/AA/6/60型病毒的全部8个基因 PATX载体，然后对每个克隆进行三到五个克隆测序 吉恩。此外，我正在对所有可用的毒力片段进行测序 Wt A/AA/6/60病毒以确定与CA病毒的哪些差异 都是有毒的wt‘s所共有的。下一步将是点突变 CA基因中的特定核苷酸被鉴定为潜在的 对致病力和突变基因重新插入到 毒力WT A/AA/6/60，以确定对这些毒力的影响 突变。

My research emphasis has been on the molecular mechanisms responsible for the attenuation and the phenotypes of cold adaptation and temperature sensitivity attributed to the live, cold adapted (ca) influenza A/AA/6/60 vaccine. I have cloned all eight genes of the wild type (wt) progenitor virus and all eight genes of caA/AA/6/60 virus into the pATX vector and have then sequenced three to five clones of each gene. In addition, I am sequencing all available virulent passages of the wt A/AA/6/60 virus to determine which differences from the ca virus are common to the virulent wt's. The next step will be site mutagenesis of specific nucleotides in the ca genes identified as potentially important to virulence and reinsertion of the mutated gene into a virulent wt A/AA/6/60 to determine the effects on virulence of those mutations.