Fish K N, Britt W, Nelson J A
Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland 97201, USA.
J Virol. 1996 Mar;70(3):1855-62. doi: 10.1128/JVI.70.3.1855-1862.1996.
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 with 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.
人巨细胞病毒（HCMV）感染单核细胞衍生的巨噬细胞（MDM）会导致病毒生长延迟且非裂解性产生。在复制后期，感染性病毒仍与细胞质空泡中的细胞相关联。为了了解HCMV在MDM中的存活和持续存在机制，我们研究了这些细胞中含HCMV空泡的形成和运输所涉及的机制。利用针对病毒和细胞蛋白的抗体进行双标记免疫荧光，含HCMV的空泡与高尔基体标记物甘露糖苷酶II相关，但与早期内体（转铁蛋白受体和rab5）或晚期内体和早期溶酶体（LAMP-1和-2）的标记物无关。此外，随着MDM中晚期病毒感染的进展，细胞在高尔基体中显示出越来越多的异常。对感染细胞结构特征的分析揭示了微管网络的破坏。这些观察结果提示了一种新机制，通过该机制HCMV在MDM中被空泡化，避免了从细胞中降解和释放。
