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UL135 and UL136 Epistasis Controls Reactivation of Human Cytomegalovirus.

Melissa A MoyDonna Collins-McMillenLindsey CrawfordChristopher ParkinsSebastian ZeltzerKatie CavinessPatrizia CaposioFelicia D Goodrum
Published in: bioRxiv : the preprint server for biology (2023)
Human cytomegalovirus (HCMV) is one of nine human herpesviruses and a significant human pathogen. While HCMV establishes a life-long latent infection that is typically asymptomatic in healthy individuals, its reactivation from latency can have devastating consequences in the immune compromised. Defining virus-host and virus-virus interactions important for HCMV latency, reactivation and replication is critical to defining the molecular basis of latent and replicative states and in controlling infection and CMV disease. Here we define a genetic relationship between two viral genes in controlling virus reactivation from latency using primary human hematopoietic progenitor cell and humanized mouse models.
Keyphrases
  • endothelial cells
  • induced pluripotent stem cells
  • pluripotent stem cells
  • gene expression
  • bone marrow
  • sars cov
  • dna methylation
  • candida albicans
  • herpes simplex virus