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Cytomegalovirus Disease01:27

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Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...
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Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates
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A systemic network triggered by human cytomegalovirus entry.

Anyou Wang1, Li Ren, Hong Li

  • 1School of Public Health, University of California, Berkeley, CA 94720, USA.

Advances in Virology
|February 8, 2012
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Summary

Human cytomegalovirus (HCMV) entry activates a complex network of cellular pathways. Systems biology reveals key protein modules and nuclear processes crucial for viral entry and infection.

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Area of Science:

  • Virology
  • Systems Biology
  • Cellular Biology

Background:

  • Virus entry is a complex, multistep process involving intricate cellular pathways.
  • The molecular details of these virus-induced cellular networks remain largely unknown.
  • Human cytomegalovirus (HCMV) is a significant opportunistic pathogen with a poorly understood entry mechanism.

Purpose of the Study:

  • To elucidate the systemic network of cellular pathways activated during HCMV entry.
  • To identify key functional modules and regulatory elements involved in the viral entry process.
  • To understand the temporal dynamics of cellular responses to HCMV infection.

Main Methods:

  • Application of systems biology approaches to analyze cellular responses.
  • Identification and characterization of functional protein modules involved in the network.
  • Temporal analysis of module activation (up- and downregulation) post-infection.

Main Results:

  • A systemic virus-entry network involving ten functional modules was identified for HCMV.
  • Cellular module activation significantly declined within 25 minutes post-infection.
  • Continuous activation of receptor, ion transport, and immune response modules; early activation of cell adhesion and skeletal movement modules.
  • Over-representation of macromolecule metabolism and chromatin remodeling modules in the upregulated network.
  • Key regulatory elements, including SLC10A1, were identified controlling the network.

Conclusions:

  • HCMV entry triggers a dynamic network of cellular processes, particularly impacting nuclear functions.
  • Specific cellular modules are activated at distinct stages of viral entry, from attachment to later events.
  • Understanding this network provides insights into HCMV pathogenesis and potential therapeutic targets.