Diseases and mechanisms of persistent DNA virus infection: latency and cellular transformation.
Diseases and mechanisms of persistent DNA virus infection: latency and cellular transformation.
复制标题
持续性 DNA 病毒感染的疾病和机制：潜伏期和细胞转化。
DOI：
10.1093/infdis/132.2.209
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发表时间：
1975
期刊：
影响因子：
--
通讯作者：
Joseph S. Pagano
中科院分区：
文献类型：
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作者：
Joseph S. Pagano
杰克逊博士、霍斯特曼博士、桑福德博士：我特别高兴能向本协会的会员和他们的客人发表讲话。我们拥有一系列引人注目的疱疹病毒：单纯疱疹病毒（HSV，1型和2型），EB病毒（EBV），巨细胞病毒（CMV，类型尚未确定）和水痘带状疱疹病毒（VZV）。在我们被感染后--从子宫内到生命的第三或第四个十年的任何时间--这六种形态相似但不同的病毒，每种病毒的病原体或基因组都会终生存在。每个基因组的分子量约为1亿道尔顿。这些障碍在很大程度上是我们轻松携带的，但有时我们的负担突然显现出来。多么不同的表现！第一个在-
Dr. Jackson, Dr. Horstmann, Dr. Sanford: it is a special pleasure to address fellow members of this Society and their guests. We harbor a remarkable array of herpesviruses: herpes simplex viruses (HSV, both type 1 and type 2), Epstein-Barr virus (EBV), cytomegaloviruses (CMV, types yet to be distinguished with certainty), and varicella-zoster virus (VZV). After we are infected--any time from in utero to the third or fourth decade of life-with these six morphologically similar yet different viruses, the agent or the genome of each persists for life. Each genome has a molecular weight of about 100 million daltons. These impedimenta for the most part we carry lightly, but at times our burden is suddenly manifest. And what diverse manifestations! The first in-