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单纯疱疹病毒对MDBK细胞持续感染的建立与鉴定

Establishment and characterization of a persistent infection of MDBK cells with herpes simplex virus.

作者信息

Mannini-Palenzona A, Bartoletti A M, Foa'-Tomasi L, Baserga M, Tognon M, Manservigi R

出版信息

Microbiologica. 1985 Apr;8(2):165-80.

PMID:2409431
Abstract

A persistent, dynamic-state infection of a variant of herpes simplex virus type 1 strain MP [HSV-1 (MP)] in MDBK cells was established without supportive measures and maintained for over three years by routine passaging of the cells at 7-9 day intervals. The infection was characterized by a cyclic pattern of monolayer damage and reconstitution, correlated with virus production, which was most evident when the interval between subcultures was intentionally prolonged and the cells were left undisturbed. Occasional periods of cell crisis, with increased virus replication and extensive cytopathology, occurred. Passaging of the cells at higher density avoided eventual loss of the culture during the most severe crises. Presence of specific antibodies did not alter the course of infection. Interferon was constantly found during periods of cell crisis; it appeared on the second day after subculture, reached a maximum in correspondance of the first peak of cytopathology, and disappeared well before the onset of the second wave of cytopathology. Addition of exogenous interferon cured the cells of infection. Defective interfering particles could not be found. Virus isolated during persistence differed from parental virus regarding plaque morphology, temperature sensitivity of growth, and electrophoretic pattern of infected cells glycoproteins. A discussion on the possible mechanisms of persistence is provided.

摘要

在无辅助措施的情况下,在MDBK细胞中建立了单纯疱疹病毒1型MP株变体[HSV-1(MP)]的持续性动态感染,并通过每隔7 - 9天对细胞进行常规传代维持了三年多。该感染的特征是单层细胞损伤和重建的周期性模式,与病毒产生相关,当亚培养间隔有意延长且细胞未受干扰时最为明显。偶尔会出现细胞危机期,伴有病毒复制增加和广泛的细胞病理学变化。在细胞密度较高时传代可避免在最严重危机期间培养物最终丢失。特异性抗体的存在并未改变感染进程。在细胞危机期持续发现干扰素;它在亚培养后第二天出现,在细胞病理学第一个峰值时达到最大值,并在第二轮细胞病理学出现之前很久就消失了。添加外源性干扰素可使细胞治愈感染。未发现缺陷干扰颗粒。持续性感染期间分离出的病毒在空斑形态、生长的温度敏感性以及感染细胞糖蛋白的电泳图谱方面与亲代病毒不同。本文提供了关于持续性可能机制的讨论。

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