Reactivation of latent CMV in transplant recipients remains a significant infectious complication of transplantation. Investigation of the cellular and molecular mechanisms by which reactivation occurs has been hampered by the lack of appropriate animal models. Here, we show that transplantation of kidneys latently infected with murine cytomegalovirus (MCMV) into NOD.Cg-Prkdc scid IL2rg tm1Wjl /Szj mice results in reactivation of latent virus in the kidney, resulting in a disseminated primary infection of the recipient. This model will be useful in elucidating mechanisms of MCMV reactivation, including the roles of injury and of spontaneous reactivation, and in testing new therapies for treatment and prevention of CMV reactivation and disease.
Pretreatment of human cytomegalovirus (HCMV) with human hyperimmune globulin (CytoGam) in human embryonic lung (HEL) fibroblast culture showed successful inhibition of infectivity, and decreased extracellular viral titers and extracellular viral DNA. CytoGam prevented HCMV from inducing intracellular activation of NF-kappaB, Sp-1, and P13-K signaling pathways and the production of immediate-early (IE), early (E), and late (L) viral proteins. CytoGam neutralization of HCMV in this cell culture model prevented the earliest known signal transduction events (NF-kappaB, Sp-1, P13-K activation) after viral specific glycoproteins bind to their cognate cell membrane receptors, suggesting that this agent contains highly effective neutralizing antibodies against HCMV.
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