Human cytomegalovirus (CMV) infections are a substantial source of morbidity and mortality in transplant recipients, and a major cause of long-term disabilities in congenitally infected children. Because of this, the development of new antiviral therapies is urgently needed. The ability of this virus to undergo lifelong latency and reactivation cycles, however, represents a formidable obstacle in our progress towards this goal. Here, we propose to use two in vitro models of CMV latency in hematopoietic cells to conclusively establish if and how maintenance of latent viral genomes is achieved in dividing myeloid progenitor cells. This work will provide significant insights into a crucial aspect of CMV latency, and will constitute the foundation for the development of innovative therapies with the potential to eradicate this virus from the human population.
Human cytomegalovirus (CMV) is a serious source of morbidity and mortality in immunocompromised individuals such as AIDS patients, transplant recipients, and newborns. Because of this, the development of novel antiviral therapies is a priority. The aim of this project is to identify the mechanisms supporting maintenance of latent viral genomes in hematopoietic progenitor cells, providing the knowledge required for the production of new therapies to block CMV's ability to persist within the human population.
|Coronel, Roxanne; Jesus, Desyree M; Dalle Ore, Lucia et al. (2016) Activation of Langerhans-Type Dendritic Cells Alters Human Cytomegalovirus Infection and Reactivation in a Stimulus-Dependent Manner. Front Microbiol 7:1445|
|Coronel, Roxanne; Takayama, Sachiko; Juwono, Timothy et al. (2015) Dynamics of Human Cytomegalovirus Infection in CD34+ Hematopoietic Cells and Derived Langerhans-Type Dendritic Cells. J Virol 89:5615-32|
|Hertel, Laura (2014) Human cytomegalovirus tropism for mucosal myeloid dendritic cells. Rev Med Virol 24:379-95|
|Lauron, Elvin J; Yu, Dong; Fehr, Anthony R et al. (2014) Human cytomegalovirus infection of langerhans-type dendritic cells does not require the presence of the gH/gL/UL128-131A complex and is blocked after nuclear deposition of viral genomes in immature cells. J Virol 88:403-16|