IDENTITY OF ATTENUATING LESIONS IN LIVE INFLUENZA VACCINE

我的研究重点一直是在分子机制负责 冷适应和温度的衰减和表型 归因于活的冷适应（ca）流感A/AA/6/60的敏感性 疫苗 我克隆了野生型（wt）祖先的所有八个基因， 病毒和caA/AA/6/60病毒的所有8个基因插入pATX载体中， 然后对每个基因的三到五个克隆进行测序。 另外我 我正在对wt A/AA/6/60病毒的所有可用毒力传代进行测序 为了确定与CA病毒的哪些差异是共同的， 有毒WT。 下一步将是对特定的 CA基因中的核苷酸被鉴定为对 毒力和突变基因重新插入到毒力野生型中 A/AA/6/60，以确定这些突变对毒力的影响。

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.