HCMV miRNA targets reveal important cellular pathways for viral replication, latency, and reactivation

Nicole L. Diggins, Meaghan Hancock

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

It is now well appreciated that microRNAs (miRNAs) play a critical role in the lifecycles of many herpes viruses. The human cytomegalovirus (HCMV) replication cycle varies significantly depending on the cell type infected, with lytic replication occurring in fully-differentiated cells such as fibroblasts, endothelial cells, or macrophages, and latent infection occurring in less-differentiated CD14+ monocytes and CD34+ hematopoietic progenitor cells where viral gene expression is severely diminished and progeny virus is not produced. Given their non-immunogenic nature and their capacity to target numerous cellular and viral transcripts, miRNAs represent a particularly advantageous means for HCMV to manipulate viral gene expression and cellular signaling pathways during lytic and latent infection. This review will focus on our current knowledge of HCMV miRNA viral and cellular targets, and discuss their importance in lytic and latent infection, highlight the challenges of studying HCMV miRNAs, and describe how viral miRNAs can help us to better understand the cellular processes involved in HCMV latency.

Original languageEnglish (US)
Article number29
JournalNon-coding RNA
Volume4
Issue number4
DOIs
StatePublished - Oct 22 2018

Fingerprint

Virus Latency
Cytomegalovirus
MicroRNAs
Viral Genes
Viruses
Gene expression
Infection
Cell signaling
Gene Expression
Macrophages
Endothelial cells
Fibroblasts
Hematopoietic Stem Cells
Monocytes
Endothelial Cells

Keywords

  • Cytomegalovirus
  • Latency
  • MiRNA

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics

Cite this

HCMV miRNA targets reveal important cellular pathways for viral replication, latency, and reactivation. / Diggins, Nicole L.; Hancock, Meaghan.

In: Non-coding RNA, Vol. 4, No. 4, 29, 22.10.2018.

Research output: Contribution to journalReview article

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