The role of human cytomegalovirus in atherosclerosis: a systematic review

Acta Biochim Biophys Sin (Shanghai). 2020 Apr 20;52(4):339-353. doi: 10.1093/abbs/gmaa005.


Atherosclerosis is a progressive vascular disease with increasing morbidity and mortality year by year in modern society. Human cytomegalovirus (HCMV) infection is closely associated with the development of atherosclerosis. HCMV infection may accelerate graft atherosclerosis and the development of transplant vasculopathy in organ transplantation. However, our current understanding of HCMV-associated atherosclerosis remains limited and is mainly based on clinical observations. The underlying mechanism of the involvement of HCMV infection in atherogenesis remains unclear. Here, we summarized current knowledge regarding the multiple influences of HCMV on a diverse range of infected cells, including vascular endothelial cells, vascular smooth muscle cells, monocytes, macrophages, and T cells. In addition, we described potential HCMV-induced molecular mechanisms, such as oxidative stress, endoplasmic reticulum stress, autophagy, lipid metabolism, and miRNA regulation, which are involved in the development of HCMV-associated atherogenesis. Gaining an improved understanding of these mechanisms will facilitate the development of novel and effective therapeutic strategies for the treatment of HCMV-related cardiovascular disease.

Keywords: atherosclerosis; human cytomegalovirus; infection; mechanism.

Publication types

  • Systematic Review

MeSH terms

  • Atherosclerosis* / metabolism
  • Atherosclerosis* / pathology
  • Atherosclerosis* / virology
  • Cytomegalovirus / metabolism*
  • Cytomegalovirus Infections* / metabolism
  • Cytomegalovirus Infections* / pathology
  • Endoplasmic Reticulum Stress*
  • Endothelial Cells / metabolism
  • Endothelial Cells / pathology
  • Endothelial Cells / virology
  • Humans
  • Lipid Metabolism*
  • Macrophages / metabolism
  • Macrophages / pathology
  • Macrophages / virology
  • MicroRNAs / metabolism
  • Monocytes / metabolism
  • Monocytes / pathology
  • Monocytes / virology
  • Oxidative Stress*
  • T-Lymphocytes / metabolism
  • T-Lymphocytes / pathology
  • T-Lymphocytes / virology


  • MicroRNAs