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The Persistence of Louping Ill Virus in Immunosuppressed Guinea-pigs

机译:在免疫抑制的豚鼠中持续感染流感病毒

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摘要

Louping ill virus proved to be pathogenic for young guinea-pigs, about 20 days old weighing about 150-180 g. In older guinea-pigs there was inapparent infection with virus replication in the brain and spleen, inflammatory lesions of encephalitis but without clinical signs or mortality. In non-immunosuppressed guinea-pigs virus replication was noted in the brain and spleen only during the first 5 to 7 days after infection. Serum antibodies appeared on the 3rd day, increased quickly and reached the maximum after 9 days, remaining at the same level for up to the 51st day. In immunosuppressed animals replication of virus in the brain was similar during the first 7 days to that of untreated guinea-pigs, but thereafter, it increased considerably reaching 105 LD50 of virus by the 15th day and later, although in diminished quantities, persisted for at least 29 days after infection. Replication of virus was not demonstrated in the spleen of immunosuppressed animals during the first 7 days, but virus appeared on the 9th day, attained a peak by the 15th day; after a slow decline it could still be detected by the 25th day. Serum neutralizing antibodies after a very short appearance between the 3rd and 5th day, declined quickly and disappeared almost completely until the 12th day. From the 15th day the amount of antibody increased reaching the top level by the 22nd day, and remained so at least until the 51st day after infection.Inflammatory and degenerative brain lesions were noted in both immunosuppressed and non-immunosuppressed animals, but whereas the curve representing inflammatory lesions followed the pattern of serum antibodies, the degenerative changes appeared to follow the pattern of virus replication. While inflammatory changes were present in non-immunosuppressed animals beginning from the 3rd day, in immunosuppressed guinea-pigs no inflammatory lesions were detected until about 12-15 days after infection. The absence of inflammatory lesions at the beginning of infection in immunosuppressed animals, coincided with the critical decline in the presence of serum antibodies. Although lesions were present in most parts of the brain the most severe and constant lesions were found invariably in the cerebellum.The successful tracing of louping ill virus by immunofluorescence proved that this method is highly sensitive and that it could be adapted for reasonably accurate quantitation of virus.
机译:流行病流行病毒被证明对年轻的豚鼠有致病性,大约20天大,重约150-180克。在较老的豚鼠中,脑和脾中病毒复制不明显,脑炎是炎性病变,但无临床体征或死亡。在非免疫抑制的豚鼠病毒中,仅在感染后的前5至7天才在大脑和脾脏中发现病毒复制。血清抗体在第3天出现,迅速增加并在9天后达到最大值,直到第51天仍保持相同水平。在免疫抑制的动物中,头7天的大脑中病毒复制与未经处理的豚鼠相似,但是此后,在第15天及以后,其病毒的LD50大大增加,达到10 5 ,尽管数量减少,但感染后至少持续29天。免疫抑制动物的脾脏在最初的7天没有显示出病毒的复制,但是在第9天出现了病毒,到第15天达到了峰值。在缓慢下降之后,到第25天仍可以检测到。在第3天到第5天之间出现非常短的时间后,血清中和抗体迅速下降,直到第12天几乎完全消失。从第15天起,抗体的量增加到22天达到最高水平,并且至少一直保持到感染后第51天。免疫抑制和非免疫抑制的动物均出现了炎症和变性脑损伤,但是曲线呈曲线。代表血清抗体模式的炎症性病变,变性变化似乎遵循病毒复制的模式。从第3天开始,非免疫抑制动物出现炎症变化,而免疫抑制的豚鼠直到感染后约12-15天才检测到炎症损伤。免疫抑制动物在感染开始时不存在炎症性病变,这与血清抗体存在的严重下降相吻合。尽管病变在大脑的大多数部位都存在,但在小脑中却始终发现最严重和恒定的病变。通过免疫荧光技术成功地检测出大块的virus病毒,证明该方法具有很高的灵敏度,可用于合理准确地定量病毒。

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