Human parvovirus B19 nonstructural protein NS1 enhanced the expression of cleavage of 70 kDa U1-snRNP autoantigen

Background: human parvovirus b19 (b19) is known to induce apoptosis that has been associated with a variety of autoimmune disorders. although we have previously reported that b19 non-structural protein (ns1) induces mitochondrial-dependent apoptosis in cos-7 cells,the precise mechanism of b19-ns1 in developing autoimmunity is still obscure. methods. to further examine the effect of b19-ns1 in presence of autoantigens,cos-7 cells were transfected with pegfp,pegfp-b19-ns1 and pegfp-ns1k334e,a mutant form of b19-ns1,and detected the expressions of autoantigens by various autoantibodies against sm,u1 small nuclear ribonucleoprotein (u1-snrnp),ssa/ro,ssb/la,scl-70,jo-1,ku,and centromere protein (cenp) a/b by using immunoblotting. results: significantly increased apoptosis was detected in cos-7 cells transfected with pegfp-b19-ns1 compared to those transfected with pegfp. meanwhile,the apoptotic 70 kda u1-snrnp protein in cos-7 cells transfected with pegfp-b19-ns1 is cleaved by caspase-3 and converted into a specific 40 kda product,which were recognized by anti-u1-snrnp autoantibody. in contrast,significantly decreased apoptosis and cleaved 40 kda product were observed in cos-7 cells transfected with pegfp-ns1k334e compared to those transfected with pegfp-b19-ns1. conclusions: these findings suggested crucial association of b19-ns1 in development of autoimmunity by inducing apoptosis and specific cleavage of 70 kda u1-snrnp. © 2010 tzang et al; licensee biomed central ltd.