Abstract
Human cytomegalovirus (HCMV) is familiar to pediatric rheumatologists mainly as a cause of opportunistic disease in pharmacologically immune suppressed patients. However, HCMV also has a variety of immuno-modulatory effects, through which it may influence the course of rheumatic conditions. In this article we discuss the interplay between HCMV and the immune system, and review the clinical manifestations, diagnosis, and treatment of HCMV infection in children with rheumatic disease.
Highlights
Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that causes symptoms primarily in immunecompromised individuals
natural killer (NK) cell function has been studied in Macrophage activation syndrome (MAS). These studies revealed that as in Hemophagocytic lymphohistiocytosis (HLH), NK cell function is impaired in approximately 50% of children with MAS [79], and more recent gene expression data have shown that NK-cell related genes are down-regulated in children with systemic onset juvenile idiopathic arthritis (SJIA) complicated by MAS [80]. These findings suggest that NK cell defects may have an important role in the pathogenesis of MAS
Summary HCMV disease may occur as a consequence of re-activation of latent virus in children receiving immunosuppressive drugs for systemic rheumatic disease
Summary
Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that causes symptoms primarily in immunecompromised individuals. Pediatric rheumatic diseases with a systemic component are characterized by increased concentrations of pro-inflammatory cytokines in the peripheral blood, [14,15,16], suggesting that the likelihood of clinically significant HCMV infection may be increased in the setting of uncontrolled rheumatic disease. Numerous other mechanisms for evasion of cell-mediated immunity have been described, including inhibition of MHC-II expression [29] and expression of a viral homologue of the naturally occurring human immunosuppressive cytokine interleukin-10 [30].
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