羊瘙痒病小鼠适应株ME7可突破种属屏障颅内感染金黄地鼠

目的　羊瘙痒病感染因子在哺乳动物种属间的传播认为受种属屏障的限制 ,研究羊瘙痒病小鼠适应株ME7在仓鼠中的发病特征。方法　ME7毒株颅内接种至金黄地鼠 ,观测疾病发生的潜伏期、临床病程和主要症状 ;Westernblot和电子显微镜动态观测脑组织中PrPSc和痒病相关纤维的出现和分子特征。结果　与以往报道的金黄地鼠适应株 2 6 3K和小鼠适应株 139A不同 ,在接种后 4 6 0～ 5 30d后 ,感染动物出现明显的症状 ,主要为消瘦、嗜睡、运动迟缓 ;感染动物脑组织中存在有羊瘙痒病相关纤维和PrP -res;羊瘙痒病相关纤维和PrP -res的出现明显早于临床发病 ;比较三种毒株在仓鼠和小鼠脑组织中出现的PrP -res发现虽然在电泳移动位置上无差异 ,但ME7和 139A的无糖分子比例明显降低。结论　小鼠适应株ME7可突破种属屏障感染金黄地鼠 ;不同毒株在潜伏期、主要临床症状和临床病程等方面有明显差异 ;PrP -res的形成不仅受接种毒株的影响 ,而且受宿主PrP分子特征的影响

Mouse-adapted scrapie strain 139A can overcome species barrier to induce spongiform encephalopathy in golden hamster

Aim Since transmission of scrapie agents among mammalian species is restricted by species barrier In this study,the infectious characteristics of the mouse adapted scrapie strain ME7 in hamster would be identified Methods Brain homogenate prepared from strain ME7 infected mice was intracerebrally inoculated into hamsters The incubation time,clinical course and main symptoms were monitored Using Western blot and electronic microscopy,presence and molecular features of protease resistant PrP (PrPres) and scrapie associated fibril (SAF) in brain tissue were dynamic observed Results Contrast to the infections of strain 263K and 139A in hamster models that we described previously,a prolonged incubation was observed in the infection of strain ME7 The clinical symptoms were clearly identified during 460 to 530 days after challenge,including severe thin,and sluggish PrPres and SAF were detected in the brain tissues from infected animals,which appeared much earlier than the onset of clinical symptoms In line with the outcome in mouse,the electrophoresis mobility of PrPres proteins from three tested scrapie strains in hamster were extremely similar,however,the ratios of unglycosylated PrPres in ME7 and 139A infected hamster brains seemed less than that in mice Conclusion Mouse adapted scrapie strain ME7 can break through species barrier to induce spongiform encephalopathy in golden hamster Different strains may have different incubation periods,clinical features,as well as clinical courses The formation of PrP Sc might depend not only on the inoculated agents,but also on the PrP molecular characteristics of the infected host