Phenotypic alterations and survival of monocytes following infection by human herpesvirus-6.
Freshly isolated monocytes rapidly undergo physiological changes in vitro, resulting in programmed cell death (apoptosis). Activation of monocytes, which promotes differentiation into macrophages, is known to inhibit apoptotic processes. In the present study, we report that human herpesvirus-6 (HHV-6) prevents monocytes from undergoing spontaneous apoptosis during the first 72 hours of culture. Furthermore, significant alterations in cell-surface phenotype were observed after 72 hours of infection with HHV-6. HHV-6-infected monocyte cultures have considerably reduced levels of CD14, CD64 (FcgammaRI) and HLA-DR antigen on their surface, while CD32 (FcgammaRII) expression is unaffected. On the basis of these results, we hypothesize that HHV-6 promotes monocytes survival and causes phenotypic modifications that could favor immune evasion and ensure its persistence within the infected host.
Laboratory of Virology, Rheumatology and Immunology Research Center, CHUL Research Center and Faculty of Medicine, Laval University, Quebec, Canada.
M-E
ME
Janelle
L
L
Flamand
D017209:Apoptosis; D002470:Cell Survival; D002478:Cells, Cultured; D015536:Down-Regulation; D006684:HLA-DR Antigens / Q000378:metabolism*; D015654:Herpesvirus 6, Human / Q000472:pathogenicity*; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000378:metabolism*; D009000:Monocytes / Q000166:cytology* / Q000821:virology; D010641:Phenotype; D017452:Receptors, IgG / Q000378:metabolism*
D006684:HLA-DR Antigens; D018950:Lipopolysaccharide Receptors; D017452:Receptors, IgG