Fennestad K L
Arch Virol. 1985;84(3-4):163-74. doi: 10.1007/BF01378969.
A pathogenetic study of pleural effusion disease (PED) in rabbits was made, using the virulent PED agent or virus (PEDV) and an avirulent derivate of this isolate. Independent of infective dose within the range examined, the virulent isolate caused fatal clinical disease, whereas the avirulent isolate caused subclinical infection. The two isolates differed in rapidity of initial spread of infection and in the maximum virus titres in serum, but they both resulted in a similar low level persisting viraemia. Circulating virulent virus gradually became avirulent during the viraemia. Avirulent infection induced protective immunity to virulent challenge during the first week after primary infection, but full clinical protection was not established until after the fourth week. The findings, corrobated with other closely comparable observations, suggest that the emergence of PED as an intercurrent mortality problem during rabbit passage of pathogenic Treponema pallidum is the result of a specific selective pressure on a benign passenger virus. The expression of virulence of PEDV appears to be dependent on length of interval between passages.
利用强毒胸膜积液病病原体或病毒(PEDV)及其无毒衍生株,对家兔胸膜积液病(PED)进行了发病机制研究。在所研究的感染剂量范围内,无论感染剂量如何,强毒株都会引发致命的临床疾病,而无毒株则会导致亚临床感染。这两种毒株在感染初期传播速度以及血清中病毒最高滴度方面存在差异,但二者均导致相似的低水平持续性病毒血症。在病毒血症期间,循环中的强毒病毒逐渐变为无毒。无毒感染在初次感染后的第一周诱导对强毒攻击的保护性免疫,但直到第四周后才建立起完全的临床保护。这些发现与其他密切相关的观察结果相互印证,表明在致病性梅毒螺旋体兔传代过程中,PED作为一种并发死亡问题的出现是对一种良性伴随病毒产生特定选择压力的结果。PEDV毒力的表达似乎取决于传代间隔时间的长短。