A novel mechanism for persistence of human cytomegalovirus in macrophages
A novel mechanism for persistence of human cytomegalovirus in macrophages
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DOI：
10.1128/jvi.70.3.1855-1862.1996
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发表时间：
1996-03-01
影响因子：
5.4
通讯作者：
Nelson, JA
中科院分区：
文献类型：
--
作者：
Fish, KN;Britt, W;Nelson, JA
人巨细胞病毒（HCMV）感染单核细胞衍生的巨噬细胞（MDM）导致延迟和非裂解性生产性病毒生长。在复制的后期，感染性病毒在细胞质空泡中保持细胞结合。为了了解HCMV在MDM中的存活和持久性，我们研究了这些细胞中含HCMV空泡形成和运输的机制。利用双标记免疫荧光与抗体的病毒和细胞蛋白，HCMV的空泡与高尔基体标记甘露糖苷酶II，但不，vith标记早期内涵体（转铁蛋白受体和rab 5）或晚期内涵体和早期溶酶体（LAMP-1和-2）。此外，随着晚期病毒感染在MDM中的进展，细胞显示高尔基体的异常增加。感染细胞的结构特征分析揭示了微管网络的破坏。这些观察结果表明，HCMV在MDM中空泡化，避免降解和从细胞释放的新机制。
Human cytomegalovirus (HCMV) infection of monocyte-derived macrophages (MDM) results in delayed and nonlytic productive viral growth. During late stages of replication, infectious virus remains cell associated in cytoplasmic vacuoles. In order to understand HCMV survival and persistence in MDM, we examined mechanisms involved in the formation and trafficking of HCMV-containing vacuoles in these cells. Utilizing double-label immunofluorescence with antibodies to viral and cellular proteins, HCMV-containing vacuoles were associated with the Golgi apparatus marker mannosidase II but not,vith markers to early endosomes (transferrin receptor and rab5) or late endosomes and early lysosomes (LAMP-1 and -2). In addition, as late-stage viral infection progressed in MDM, the cells displayed increasing abnormalities in the Golgi apparatus. Analysis of structural features of infected cells revealed the disruption of the microtubule network. These observations suggest a novel mechanism by which HCMV is vacuolized in MDM, avoiding degradation and release from the cell.