鸡传染性法氏囊病病毒弱毒株在鸡体连续传代后毒力增强的分子机理研究

Study on the Molecular Mechanism of Increased Virulence of IBDV Attenuated Strains by Serial Passage in Chickens

关键词:  传染性法氏囊病病毒  毒力增强  VP2蛋白  分子机理

Key words:  IBDV  virulence enhance  VP2 protein  molecular mechanism

摘要:

将两株鸡传染性法氏囊病病毒（IBDV）弱毒株在SPF鸡体内连续传代至第5、第6代时，出现明显的法氏囊萎缩和B∶B指数下降，表明IBDV弱毒株在鸡体内连续传代后毒力增强。为进一步阐释哪些基因位点导致了上述毒力的变化，本试验测定了基础弱毒株及其在鸡体内传代后各个代次毒的基因组序列，比对分析后发现VP2蛋白253位氨基酸发生了由H到Q或N的变异，表明VP2蛋白253位氨基酸的替换可能会增强传染性法氏囊病病毒在鸡体内的致病性。

Abstract:

Two attenuated IBDV strains were passaged five or six times in SPF chickens. Both attenuated strains increased in virulence during the passage in susceptible chickens as evidenced by the decrease in bursa/body weight ratios and B∶B index. In order to further explain which animo acids result in the change of virulence, sequences of the genome of the attenuated IBDV strains and the passage strains in chickens were amplified and analyzed. The results showed that an amino acid mutated from Histidine(H) to Glutamine(Q) or Asparagine(N) at position 253 in VP2 during the passage in chickens. Together ,the pathogenicity and molecular data indicate that a single amino acid substitution at position 253 in VP2 increases the pathogenicity of IBDV in vivo.