| Objective:To explore the relationship between Epstein Barr virus(EBV)latent membrane protein 1(LMP1),latent membrane protein 2(LMP2)and the clinical characteristics of systemic lupus erythematosus(SLE),and its profile of Epstein Barr virus(EBV)infection in patients.Methods:In-patients with SLE who were newly-onset and treatment-na(?)ve in Department of Rheumatology,the Affiliated Hospital of Qingdao University,between October 2020 and September 2022 were screened consecutively.Serum antibodies of EBV antigens specifically expressed in different infection status were detected,including anti-VCA-IgG,-IgM and-IgA,anti-EA-IgA,anti-EBNA1,anti-LMP1,anti-LMP2,anti-EBNA2,and anti-EBNA3 antibodies.The differences of EBV infection profile were compared between SLE patients and the controls,as well as the clinical characteristics between the status of EBV infection and the status of EBV antibodies.Results:A total of 42 patients with SLE were enrolled,with 5(11.9%)males and an average age of 32(26,43)years.Among them,3(7.1%)cases were with EBV previous infection,6(14.3%)cases were with lytic infection,and 36(85.7%)cases were with pure latent infection.There were no differences of the clinical characteristics between patients of lytic infection and latent infection(P>0.05).There were 37 cases(88.1%)with EBV latent infections(including one patient with lytic infection overlap),among which 20(47.6%)cases were with Latency Ⅰ,11(26.2%)cases were with Latency Ⅱ,and 6 cases(14.3%)were with Latency Ⅲ.Patients with Latency Ⅱ infection had more kidney involvements(90.9%vs 35%,χ~2=8.976,P=0.006)and higher SLEDAI(13±3 vs 7±4,F=10.950,P=0.002)than patients with Latency Ⅰ,and more digestive system involvements than patients with Latency Ⅲ(54.5%vs 0%,χ~2=5.069,P=0.031);Patients with Latency Ⅲ had higher serum IgA than patents with Latency Ⅰ(3.04[2.72,5.66]g/L vs 2.29[1.58,2.84]g/L,H=7.311,P=0.026).Patients with anti-LMP1 were 19%,who were with more renal involvements(100%vs 50%,χ~2=6.720,P=0.028),more nervous system involvements(25%vs 0%,χ~2=8.925,P=0.033)and lower CD4~+T cell counts(146[108,301]/uL vs 340[234,508]/uL,Z=-1.986,P=0.047)than patients without;Patients with anti-LMP2 were 26.2%,who were with more musculoskeletal involvements(72.7%vs 32.3%,χ~2=5.430,P=0.048),higher serum IgG(20.6[17.5,36.8]g/L vs 14.4[11.7,18.9]g/L,Z=-2.747,P=0.006),higher IgA(2.94[2.58,4.51]g/L)vs2.29[1.66,3.24]g/L,Z=-2.217,P=0.027),higher serum IgM(1.64[1.08,2.30]g/L vs0.84[0.50,1.07]g/L,Z=-3.220,P=0.001)and higher ESR(46[19.6,102]mm/h vs19[11.2,37]mm/h,Z=-2.346,P=0.019);Patients with anti-EBNA1 were 88.1%,who were with higher anti-Ro52 positive rate(57.1%vs 0%,χ~2=7.568,P=0.023)and higher serum IgM(0.97[0.64,1.65]vs 0.53[0.36,0.64],Z=-2.351,P=0.019)compared with patients without.In SLE patients,anti LMP1 was significantly positively correlated with SLEDAI(r=0.506,P=0.001),anti-LMP2,EBNA1 was slightly positively correlated with IgM(r=0.323,P=0.037;r=0.348,P=0.024),and anti-LMP1,LMP2,and EBNA1 were not significantly correlated with eGFR(r=-0.213,P=0.176;r=-0.058,P=0.716;r=-0.017,P=0.916).Conclusions:The EBV latent infection antigens EBNA1,LMP1 and LMP2 may be involved in the development of SLE. |
PDF Full Text Request