期刊
JOURNAL OF VIROLOGY
卷 82, 期 13, 页码 6524-6535出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00502-08
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- NCRR NIH HHS [RR00163, K01 RR000163, P51 RR000163] Funding Source: Medline
- NHLBI NIH HHS [R01 HL083194, R01 HL088603, HL65754, HL 66238-01, R01 HL065754, R01 HL066238, R01 HL088603-04, R01 HL085451, HL083194, HL71695, R01 HL071695] Funding Source: Medline
- NIAID NIH HHS [R01 AI021640, AI21640] Funding Source: Medline
Human cytomegalovirus (HCMV) is implicated in the acceleration of a number of vascular diseases including transplant vascular sclerosis (TVS), the lesion associated with chronic rejection (CR) of solid organ transplants. Although the virus persists in the allograft throughout the course of disease, few cells are directly infected by CMV. This observation is in contrast to the global effects that CMV has on the acceleration of TVS/CR, suggesting that CMV infection indirectly promotes the vascular disease process. Recent transcriptome analysis of CMV-infected heart allografts indicates that the virus induces cytokines and growth factors associated with angiogenesis (AG) and wound healing (WH), suggesting that CMV may accelerate TVS/CR through the induction and secretion of AG/WH factors from infected cells. We analyzed virus-free supernatants from HCMV-infected cells (HCMV secretomes) for growth factors, by mass spectrometry and immunoassays, and found that the HCMV secretome contains over 1,000 cellular proteins, many of which are involved in AG/WH. Importantly, functional assays demonstrated that CMV but not herpes simplex virus secretomes not only induce AG/WH but also promote neovessel stabilization and endothelial cell survival for 2 weeks. These findings suggest that CMV acceleration of TVS occurs through virus-induced growth factors and cytokines in the CMV secretome.
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