Abstract
Renal transplant recipients (RTR) display high burdens of cytomegalovirus (CMV) and accelerated cardiovascular change. NK cells can control CMV and may contribute to vascular pathologies. Polymorphisms in genes encoding the inhibitory receptor LILRB1 and its ligand HLA-G, and the activating receptor NKG2C may illuminate the role of NK cells in vascular health and CMV immunity.We assessed 81 healthy adults and 82 RTR >2 years after transplantation. RTR had higher humoral and T-cell responses to CMV, and impaired vascular health. A 14bp indel in HLA-G associated with increased flow-mediated dilatation of the brachial artery. The T allele of LILRB1 rs1061680 associated with increased carotid intimal media thickness (cIMT) in RTR and controls. A 16 kb deletion encompassing the NKG2C gene associated with lower cIMT values and higher humoral and T-cell responses to CMV. Hence all polymorphisms tested had small but discernable effects on vascular health. The NKG2C deletion may act via CMV.
Highlights
Infections with cytomegalovirus (CMV) are very common – 40-90% of all adults are CMV seropositive [1]
4.0 Results and Discussion 4.1 Controls and Renal transplant recipients (RTR) were matched demographically and genotype frequencies did not differ Eighty-two RTR and 81 healthy controls were screened for polymorphisms in the genes encoding human leucocyte antigen (HLA)-G, LILRB1 and NKG2C, cardiovascular health and CMV-reactive antibodies
RTR had lower flow mediated dilatation (FMD) values (p
Summary
Infections with cytomegalovirus (CMV) are very common – 40-90% of all adults are CMV seropositive [1]. Infections are usually asymptomatic in healthy individuals, but the virus becomes latent and persists with periodic reactivations generating immune activation and accelerated T-cell differentiation [2]. CMV is implicated in the progression of several diseases of aging. Evidence linking persistent CMV with vasculopathy includes CMV-DNA in tissues removed during surgery for abdominal aortic aneurysm [3]. High CMV antibody titres are linked with increased blood pressure in young men [4] and coronary artery disease requiring surgery [5]. Proposed mechanisms include direct effects of proteins encoded by CMV, such as HCMV US28 – a chemokine receptor homologue that mediates monocyte attachment to endothelial cells [6]
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