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静脉感染后,痘苗病毒在先天抗性和易感小鼠主要靶器官中的复制

Ectromelia virus replication in major target organs of innately resistant and susceptible mice after intravenous infection.

作者信息

Brownstein D G, Bhatt P N, Gras L

机构信息

Section of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut.

出版信息

Arch Virol. 1993;129(1-4):65-75. doi: 10.1007/BF01316885.

Abstract

The kinetics of ectromelia virus replication in the spleen and liver and of alpha/beta interferon production in the spleen were determined during the first 3 days after intravenous infection with the virulent Moscow strain in resistant C57 BL/6 and susceptible DBA/2 mice. Virus replication in the spleen as measured by assays for virus DNA and infectious centers was suppressed in C57BL/6 mice relative to DBA/2 mice within the first 1 or 2 days of infection. Infectious centers increased in DBA/2 mice but not in C57 BL/6 mice. Differences in virus replication between strains were less discrete when spleens were assayed for infectious virus than when they were assayed for infectious centers because infectious centers of most C57 BL/6 mice had more infectious virus than infectious centers of DBA/2 mice. Virus replication in the liver, the major target organ, as measured by virus DNA and infectious virus assays, was suppressed in C57 BL/6 mice relative to DBA/2 mice 3 days after infection but not before that interval. The results indicate that genetic control of ectromelia virus replication begins within the first 1 or 2 days of infection in the spleen but is delayed in the liver and that genetic control is directed at the prevention of virus spread more than at virus replication.

摘要

在用强毒力的莫斯科株静脉感染抗性C57 BL/6小鼠和易感DBA/2小鼠后的头3天,测定了脾脏和肝脏中埃可病毒的复制动力学以及脾脏中α/β干扰素的产生情况。在感染后的头1或2天内,相对于DBA/2小鼠,通过病毒DNA和感染中心检测法测定的C57BL/6小鼠脾脏中的病毒复制受到抑制。DBA/2小鼠中的感染中心增加,而C57 BL/6小鼠中则没有。当检测脾脏中的感染性病毒时,不同品系之间的病毒复制差异不如检测感染中心时那么明显,因为大多数C57 BL/6小鼠的感染中心比DBA/2小鼠的感染中心含有更多的感染性病毒。通过病毒DNA和感染性病毒检测法测定,在感染后3天,相对于DBA/2小鼠,主要靶器官肝脏中的病毒复制在C57 BL/6小鼠中受到抑制,但在此之前没有。结果表明,埃可病毒复制的遗传控制在感染后的头1或2天内在脾脏中开始,但在肝脏中延迟,并且遗传控制更多地是针对防止病毒传播而不是病毒复制。

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