Abstract
Pericytes are multipotent cells of the vascular system with cytoplasmic extensions proximal to endothelial cells that occur along the abluminal surface of the endothelium. The interactions between endothelial cells and pericytes are essential for proper microvascular formation, development, stabilization, and maintenance. Pericytes are essential for the regulation of paracellular flow between cells, transendothelial fluid transport, angiogenesis, and vascular immunosurveillance. They also influence the chemical composition of the surrounding microenvironment to protect endothelial cells from potential harm. Dysregulation or loss of pericyte function can result in microvascular instability and pathological consequences. Human pericytes have been shown to be targets for human cytomegalovirus (HCMV) infection and lytic replication that likely contribute to vascular inflammation. This review focuses on human vascular pericytes and their permissiveness for HCMV infection. It also discusses their implication in pathogenesis in the blood–brain barrier (BBB), the inner blood–retinal barrier (IBRB), the placenta–blood barrier, and the renal glomerulus as well as their potential role in subclinical vascular disease.
Highlights
Pericytes, known as Roget cells or mural cells, were first described by Eberth and Rouget in the 1870s
The inner blood–retinal barrier (IBRB) consists of retinal microvascular endothelial cells covered with tightly associated pericytes and Müller cells; together, they make up the retinal vascular unit (RVU) [12]
The studies described in this review reported evidence of complete lytic replication of human cytomegalovirus (HCMV) in the brain, retinal, placental, and glomerular, pericytes populations that resulted in the induction of pro-inflammatory cytokines that likely contributed to vascular inflammation
Summary
Known as Roget cells or mural cells, were first described by Eberth and Rouget in the 1870s. Morphology, and function, depending on their organ-derived vascular bed They are located abluminal to microvascular endothelial cells with which they share a common basement membrane [6,7]. The studies described in this review reported evidence of complete lytic replication of human cytomegalovirus (HCMV) in the brain, retinal, placental, and glomerular (mesangial cells), pericytes populations that resulted in the induction of pro-inflammatory cytokines that likely contributed to vascular inflammation. These studies relied mainly on in vitro data obtained from experiments using primary cells at low passage and infection at low multiplicity. Results from these studies support the notion that all pericytes populations, regardless of origin, are permissive for HCMV infection, and that loss of HCMV immune surveillance or intermittent viral shedding over time could contribute to pericyte loss or dysfunction, microvascular instability, and subclinical progressive vascular diseases
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