A novel mechanism for persistence of human cytomegalovirus in macrophages.
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.
Fish
K N
KN
Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland 97201, USA.
Britt
W
W
Nelson
J A
JA
D000818:Animals; D002462:Cell Membrane; D002478:Cells, Cultured; D003587:Cytomegalovirus / Q000502:physiology*; D006056:Golgi Apparatus / Q000821:virology; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D006801:Humans; D008264:Macrophages / Q000276:immunology / Q000821:virology*; D008870:Microtubules / Q000821:virology; D011817:Rabbits; D014617:Vacuoles / Q000821:virology; D017735:Virus Latency; D014779:Virus Replication
D000949:Histocompatibility Antigens Class II