Chuvakova Z K, Ismailova Iu S, Kim E V, Mukazhanova G N, Zuev V A
Vopr Virusol. 1993 Jan-Feb;38(1):2-6.
Influenza A/H1N1 (serovariant Hsw1N1) virus, a sum of isolated glycoproteins, separately neuraminidase "heads", inoculated into white random-bred female mice, induced in some of the offsprings the pathology clinically and pathomorphologically similar to previously described slow virus infection. At the same time, the pathology in the offsprings caused by the antigenic virus variant under study was characterized by complete absence of fur and more dynamic progress of the disease. It is quite obvious that glycoproteins, particularly neuraminidase, are the molecular biological basis of dystrophic and degenerative changes in the organs of baby mice due to desialization and increased fluidity of capillary endothelium membranes and, possibly, CNS and other organ cells.
甲型H1N1流感病毒（血清变异型Hsw1N1），即一组分离出的糖蛋白，分别是神经氨酸酶“头部”，接种到白色随机繁殖的雌性小鼠体内，在一些后代中诱发了临床和病理形态学上与先前描述的慢病毒感染相似的病变。同时，所研究的抗原性病毒变异体在后代中引起的病变特征是完全无毛且疾病进展更为迅速。很明显，糖蛋白，尤其是神经氨酸酶，是幼鼠器官发生营养不良和退行性变化的分子生物学基础，这是由于去唾液酸化以及毛细血管内皮细胞膜、可能还有中枢神经系统和其他器官细胞的流动性增加所致。
