Abstract
Human cytomegalovirus (HCMV) represents a prototypic pathogenic member of the β-subgroup of the herpesvirus family. A range of HCMV features like its lytic replication in multiple tissues, the lifelong persistence through periods of latency and intermitting reactivation, the extraordinary large proteome, and extensive manipulation of adaptive and innate immunity make HCMV a high profile candidate for involvement in autoimmune disorders. We surveyed the available literature for reports on HCMV association with onset or exacerbation of autoimmune disease. A causative linkage between HCMV and systemic lupus erythematosus (SLE), systemic sclerosis (SSc), diabetes mellitus type 1, and rheumatoid arthritis (RA) is suggested by the literature. However, a clear association of HCMV seroprevalence and disease could not be established, leaving the question open whether HCMV could play a coresponsible role for onset of disease. For convincing conclusions population-based prospective studies must be performed in the future. Specific immunopathogenic mechanisms by which HCMV could contribute to the course of autoimmune disease have been suggested, for example, molecular mimicry by UL94 in SSc and UL83/pp65 in SLE patients, as well as aggravation of joint inflammation by induction and expansion of CD4+/CD28− T-cells in RA patients. Further studies are needed to validate these findings and to lay the grounds for targeted therapeutic intervention.
Highlights
Autoimmune disease (AID) is a complex dysregulation of immunity, resulting in loss of self-tolerance and subsequent assault on endogenous tissue or cells
According to the studies evaluated here, there is no evidence that Human cytomegalovirus (HCMV) plays a role for the onset of type 1 diabetes (T1D) and multiple sclerosis (MS)
Concerning systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) it cannot be ruled out that HCMV may play an active role in the induction of disease depending on largely unknown genetic factors
Summary
Autoimmune disease (AID) is a complex dysregulation of immunity, resulting in loss of self-tolerance and subsequent assault on endogenous tissue or cells. A frequently discussed phenomenon in the case of turning the immune system against self-epitopes is “molecular mimicry” [11, 12] According to this concept pathogenic foreign epitopes are highly similar to host determinants and, after activation of the immune system result in self-attack. The search for published data was performed using the PubMed database and entering the keywords “cytomegalovirus” and “autoimmunity.” The autoimmune diseases, which were found most often in combination with both keywords, were searched again in combination with cytomegalovirus alone These diseases were systemic lupus erythematosus (SLE), systemic sclerosis (SSc), type 1 diabetes (T1D), multiple sclerosis (MS), and rheumatoid arthritis (RA)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
