Correlation between cytomegalovirus infection and Raynaud's phenomenon in lupus nephritis

Relationships between viruses and autoimmune diseases such as systemic lupu s erythematosus (SLE) are still elusive. Recent reports demonstrated the as sociation of some viral infections with peculiar clinical events in the gen eral population, such as cytomegalovirus (CMV) with arterial damage and Par vovirus B19 (PV-B19) with hematologic abnormalities. We planned to look for this kind of viral imprinting in SLE, hypothesizing that traces of specifi c features of some viral infections might be found in some subsets of serop ositive SLE patients. In 60 SLE patients recruited at our nephrologic cente r, serology for CMV, PV-B19, Epstein-Barr virus viral capsid antigen (EBV-V CA), Epstein-Barr nuclear antigen (EBNA) and Epstein-Barr virus early antig en (EBV-EA) was performed. chi(2) and ANOVA were employed to compare the fr equency and titers of antiviral antibodies in SLE patients with groups of t ransplant, hemodialysis and blood donor subjects. chi(2), Fisher's test, Bo nferroni and Scheffe's test were employed to compare the different biochemi cal/clinical features between seropositive and seronegative SLE patients. U nivariate and multivariate analysis (logistic regression models) were emplo yed to evaluate the odds ratio (OR) of different risk factors for vascular events (including Raynaud's phenomenon, deep venous thrombosis) and hematol ogic abnormalities (including severe anemia, leukopenia and thrombocyeopeni a). Anti-CMV (82%), anti-PV-B19 (60%), anti-EBV-VCA (92%) and EBV-EA (45%) IgG antibodies were frequent in SLE, with higher prevalence in comparison w ith the blood donor group and higher titers in comparison with transplant a nd hemodialysis groups. CMV seropositivity was a highly significant risk fa ctor for Raynaud's phenomenon (OR +alpha in univariate and multivariate ana lysis = 13.51 using a correction of 0.5 in case of a zero event), but not f or venous vascular events (OR = 1.31). An increased though not significant risk factor was found for antiphospholipid antibodies (OR = 2.71, p = 0.19) , while the presence of nephrotic syndrome during the follow-up was a signi ficant protective factor (OR = 0.15, p = 0.035). There was no significantly increased OR for PV-B19 seropositivity in cases with severe anemia (OR = 2 .09, p = 0.29). No significant associations were found with the status of E BV reactivation. In conclusion, our results support the hypothesis that vir al infection may imprint the course of SLE leading to specific clinical sub sets (i.e. CMV and 'vascular' SLE, with more frequent Raynaud's phenomenon and a less frequent typical histological renal picture responsible for neph rotic syndrome). Further prospective studies are justified to validate thes e correlations, mainly dealing with associations between acute viral infect ions and vascular events, thus eventually leading to a better understanding of mutual relationships between viruses and SLE.