Krieger J N, Scherer W F, Wiebe M E, Pancake B A, Harsanyi Z P
Infect Immun. 1979 Sep;25(3):873-9. doi: 10.1128/iai.25.3.873-879.1979.
Pathogenicities of 10 temperature-sensitive mutants of Venezuelan encephalitis virus were studied using the hamster model of human virulence. The parental strain and nine of the temperature-sensitive mutants produced lethal infections in hamsters. Strain ts 126 showed reduced hamster virulence. Deaths with the lethal mutants usually occurred 1 to 3 days later than with parental virus. Nine mutants produced lower levels of viremia than parental virus. Attenuation of ts 126 was related to restriction of viral growth in spleen and probably bone marrow and to absence of the usual pathological lesions in hemopoietic tissues and brain, but was functionally unrelated to temperature sensitivity since temperatures of both normal and infected hamsters remained within the permissive range of the mutant. Deaths did not correlate with titers of the 10 mutants in blood at permissive temperatures or with reversions of four temperature-sensitive mutants to non-temperature-sensitive virus in hamsters.
利用人类毒力的仓鼠模型研究了委内瑞拉脑炎病毒10个温度敏感突变株的致病性。亲代毒株和9个温度敏感突变株在仓鼠中引发了致死性感染。ts 126株对仓鼠的毒力降低。致死性突变株导致的死亡通常比亲代病毒晚1至3天出现。9个突变株产生的病毒血症水平低于亲代病毒。ts 126株的减毒与病毒在脾脏以及可能在骨髓中的生长受限有关,也与造血组织和大脑中通常的病理损伤缺失有关,但在功能上与温度敏感性无关,因为正常仓鼠和感染仓鼠的体温都保持在该突变株的允许温度范围内。死亡情况与10个突变株在允许温度下血液中的滴度无关,也与4个温度敏感突变株在仓鼠体内回复为非温度敏感病毒无关。