Specifically, immunopathogenic mechanisms by which HCMV could contribute to the course of autoimmune disease have been indicated, for example, molecular mimicry by the UL94 antigen in SSc patients and UL83/pp65 in SLE patients, as well as aggravation of joint inflammation by induction and expansion of CD4+/CD28− T-cells in HCMV infected RA patients. This evidence concerns the gene CD28 and rheumatoid arthritis.