IDENTITY OF ATTENUATING LESIONS IN LIVE COLD-ADAPTED INFLUENZA VACCINE

我的研究重点一直是在分子机制负责 对于冷适应的衰减和表型， 温度敏感性归因于活的，冷适应的（ca） 流感A/AA/6/60疫苗。 我克隆了野生动物的全部八个基因 型（wt）祖病毒和caA/AA/6/60病毒的所有八个基因， pATX载体，然后对每个载体的三到五个克隆进行测序， 基因 另外，我正在对所有可用的 野生型A/AA/6/60病毒，以确定与病例的差异 病毒是致命野生型常见的。 下一步将是网站 CA基因中特定核苷酸的诱变被鉴定为 对突变基因的毒力和重新插入可能重要 加入到毒性wt A/AA/6/60中，以确定 这些突变。

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.