利用病毒血清學法、聚合脢連鎖反應、南方墨點法分析被人類微小病毒B19感染的血清。血清來源為72位有紅斑性狼瘡病人；23位為風顯性關節炎；18位為修格連氏症候群；8位為雷諾氏症；5位為原發性膽汁性肝硬化；4位為傳染性紅斑；另外22位正常控制組。72位紅斑性狼瘡中有7位及4位傳染性紅斑病人有3位偵測到有人類微小病毒B19 DNA，而在其它系統性風濕性疾病無此發現。17位有B19 DNA的病人，血清內只含一種抗B19的IgG抗體及二種IgM抗體，另外55位未被B19感染的紅斑性狼瘡病人有27位測得抗B19的IgG抗體及21位有抗B19的IgM抗體。所有傳染性紅斑病人皆有抗B19的IgG及IgM抗體。由統計資料可知紅斑性狼瘡病人沒產生抗B19抗體含有B19 DNA的機率比產生抗B19抗體者高（P<0.05）。紅斑性狼瘡病人被B19感染而沒產生抗B19抗體乃因為疫系統發育不全或服用免疫抑制藥物。臨床上發現紅斑性狼瘡病人有B19 DNA存在。低補體症者被感染B19的病毒血症的盛行率比未感染者高。 Sera from 72 patients with systemic lupus erythematosus (SLE), 23 patients with rheumatoid arthritis (RA), 18 patients with Sjogren's syndrome (SS), eight patients with Raynaud's phenomenon (RP), five patients with primary biliary cirrhosis (PBC), five patients with polymyositis (PM), four patients with erythema infectiosum (EI), and 22 normal controls were examined for parvovirus B19 (B19) infection by serological assays, nested PCR, and Southern blotting. Parvovirus B19 DNA was detected in 17 of 72 patients with SLE, and in three of four patients with EI, but not detected in patients with other systemic rheumatic diseases. Of the 17 patients with B19 DNA, only one had IgG anti-B19 antibody and two with IgM anti-B19 antibodies, whereas IgG and IgM anti-B19 antibodies were detected in 27 (49.1%) and 21 (38.2%) of 55 SLE patients without B19 DNA, respectively. All sera from the patients with EI contained both IgG and IgM anti-B19 antibodies. B19 DNA was found more common in sera from SLE patients without anti-B19 antibodies than these with anti-B19 antibodies (p<0.05). The infection of B19 in patients with SLE may be due to lack of anti-B19 antibodies because of the immunocompromised host or immunosuppressive drugs. The clinical significance of the presence of B19 DNA in patients with SLE was studied. There was a higher prevalence of hypocomplementemia and Raynaud's phenomenon in patients with parvovirus.
