Abstract
Human cytomegalovirus (CMV) is a ubiquitous DNA virus that causes severe disease in patients with immature or impaired immune systems. During active infection, CMV modulates host immunity, and CMV-infected patients often develop signs of immune dysfunction, such as immunosuppression and autoimmune phenomena. Furthermore, active viral infection has been observed in several autoimmune diseases, and case reports have linked primary CMV infection and the onset of autoimmune disorders. In addition, CMV infection promotes allograft rejection and graft-versus-host disease in solid organ and bone marrow transplant recipients, respectively, further implicating CMV in the genesis and maintenance of immunopathological phenomena. The mechanisms by which CMV could induce inhibition of host defense, inflammation, and autoimmunity are discussed, as is the treatment of virus-induced immunopathology with antivirals.
Highlights
Human cytomegalovirus (CMV) is a ubiquitous DNA virus that causes severe disease in patients with immature or impaired immune systems
Such a phenomenon has clinical implications for infected patients, as demonstrated in transplant recipients-autoantibodies mediate the development of graft-versus-host disease (GVHD) in CMV-infected allogeneic stem cell transplant (alloSCT) patients and graft rejection in solid organ recipients [34,35,38,39] (Figure 2)
CMV can accelerate the progression of autoimmune disorders by mimicking autoimmunemediated tissue destruction and aggravating inflammation
Summary
During acute CMV infection, patients often suffer from immunological dysfunctions. Autoimmune phenomena are common in CMV-infected patients, and various autoantibodies have been detected in patients with systemic CMV infection [32,33,34,36,37,42]. Nonspecific hyperactivation of humoral immunity can impede the development of specific B cell responses-a potential mechanism of viral immune evasion Such a phenomenon has clinical implications for infected patients, as demonstrated in transplant recipients-autoantibodies mediate the development of GVHD in CMV-infected alloSCT patients and graft rejection in solid organ recipients [34,35,38,39] (Figure 2). Local viral replication is associated with chronic perivascular inflammation in solid organ transplant recipients (Figure 2) In these patients, CMV persists in the allograft, but few cells are infected directly by CMV. CMV persists in the allograft, but few cells are infected directly by CMV These findings contrast the global effects that CMV has on the acceleration of vascular stenosis and chronic rejection, suggesting that CMV does not promote vascular disease through direct infection of vessels; instead, it likely acts by indirect mechanisms that in part involve the immune system [179]. Abbreviations (alloSCT): allogeneic stem cell transplant; (ANCA): antineutrophil cytoplasmic antibody; (APC): antigen presenting cell; (BMT): bone marrow transplant recipient; (CMV): human cytomegalovirus; (CVID): common variable immunodeficiency; (DC): dendritic cell; (E): early; (EBV): Epstein-Barr virus; (GVHD): graft-versus-host disease; (HCV): hepatitis C virus; (HHV): human herpes virus; (IBD): inflammatory bowel disease; (IE): immediate early; (IFN): interferon; (L): late; (MHC): major histocompatibility complex; (Mj): macrophage; (NF-kB): nuclear factor-kB; (NK): natural killer; (PTDM): posttransplant diabetes mellitus; (PTLD): post-transplant lymphoproliferative disorder; (RA): rheumatoid arthritis; (SLE): systemic lupus erythematosus; (SMC): smooth muscle cell; (TLR): toll-like receptor; (TNF): tumor necrosis factor; (UC): ulcerative colitis
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