Key result
Transplanting MCMV-infected kidneys into immunodeficient mice triggers latent viral reactivation and disseminated primary infection.
Why the study?
Investigation of cellular and molecular mechanisms of CMV reactivation after transplantation has been hampered by the lack of appropriate animal models.
This novel mouse model of CMV transmission via kidney transplantation provides a tool to study mechanisms of viral reactivation and test new therapies.
Alerts to possible CMV reactivation risk in immunodeficient kidney recipients; leaves open human validation and therapy testing.
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.
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Li et al. (2012) studied CMV transmission following kidney transplantation. Transplantation of kidneys latently infected with murine cytomegalovirus (MCMV) was evaluated on Reactivation of latent virus in the kidney resulting in a disseminated primary infection. Transplantation of kidneys latently infected with murine cytomegalovirus into immunodeficient mice resulted in reactivation of latent virus and disseminated primary infection.
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