期刊
JOURNAL OF VIROLOGY
卷 81, 期 20, 页码 10879-10889出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00504-07
关键词
-
类别
资金
- NCI NIH HHS [CA119298-01, R01 CA119298] Funding Source: Medline
- NHLBI NIH HHS [U01 HL066949, HL066949-01] Funding Source: Medline
- NINDS NIH HHS [R01 NS044323, NS44323-04] Funding Source: Medline
Equine herpesvirus type 1 (ERV-1), a member of the Alphaherpesviridae, displays a broad host range in vitro, allowing for detailed study of the mechanisms of productive infection, including attachment and entry, in various cell culture systems. Previously, we showed that ERV-1 infects Chinese hamster ovary (CHO-K1) cells even though these cells do not express a known alphaherpesvirus entry receptor. In this report, we show by electron microscopy and an infectious recovery assay that entry into CHO-K1 cells occurs via an endocytic or phagocytic mechanism, while entry into equine dermal (ED) or rabbit kidney (RK13) cells occurs by direct fusion at the cell surface. In both cases (endocytic/phagocytic or direct fusion), entry leads to productive infection. Using drugs that inhibit clathrin-dependent or caveola-dependent endocytosis, we showed that ERV-1 entry into CHO-K1 cells does not require clathrin or caveolae. We also show that ERV-1 infection requires the activation of cell signaling molecules. In particular, we demonstrate that activation of the serine/threonine Rho kinase ROCK1 is critical for infection. Inhibition of this kinase by drugs or overexpression of a negative regulator of ROCK1 significantly blocked ERV-1 infection. These results show that ERV-1 can enter disparate cell types by at least two distinct mechanisms and that productive infection is dependent upon the activation of ROCK1.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据