Frickhofen N, Abkowitz J L, Safford M, Berry J M, Antunez-de-Mayolo J, Astrow A, Cohen R, Halperin I, King L, Mintzer D
National Heart, Lung, and Blood Institute, Bethesda, Maryland.
Ann Intern Med. 1990 Dec 15;113(12):926-33. doi: 10.7326/0003-4819-113-12-926.
To determine the role of B19 parvovirus in red cell aplasia of patients infected with human immunodeficiency virus type 1 (HIV-1).
Uncontrolled clinical trial, with assay of serum, peripheral blood cells, and bone marrow for virus using DNA hybridization and immunocytochemistry techniques; these assays were then correlated with clinical findings, results of immunoassays for antivirus antibodies, and with immunoglobulin (Ig) therapy.
Government medical referral center, and university and private hospitals.
Seven patients with pure red cell aplasia and serologic evidence of infection with HIV-1.
All patients had giant pronormoblasts in the bone marrow (present in transient aplastic crisis caused by acute B19 parvovirus infection). High concentrations of B19 parvovirus were demonstrated in sera, in several cases in samples separated by weeks or months. Viral DNA and capsid protein were present in the bone marrow of three patients studied, and active viral replication was detected by southern analysis. There was no antivirus IgG in capture immunoassay and no or very low levels of antivirus IgM. The patients did not have symptoms of fifth disease, the illness caused by this virus in immunologically normal persons. Six patients were treated with a regimen of intravenous commercial immunoglobulin. In all cases, this therapy resulted in rapid reduction in serum virus concentrations and full recovery of erythropoiesis. Relapses in two cases were predicted by DNA hybridization studies, and these cases were successfully retreated.
The B19 parvovirus is a remediable cause of severe chronic anemia in HIV-infected patients. Recognition of and therapy for parvovirus in this population will avoid erythrocyte transfusion and should prevent transmission of the virus to other persons, including immunosuppressed persons and women of child-bearing age.
确定B19细小病毒在1型人类免疫缺陷病毒(HIV-1)感染患者红细胞再生障碍中的作用。
非对照临床试验,采用DNA杂交和免疫细胞化学技术检测血清、外周血细胞和骨髓中的病毒;然后将这些检测结果与临床发现、抗病毒抗体免疫测定结果以及免疫球蛋白(Ig)治疗结果相关联。
政府医疗转诊中心、大学医院和私立医院。
7例患有纯红细胞再生障碍且有HIV-1感染血清学证据的患者。
所有患者骨髓中均有巨大早幼红细胞(存在于急性B19细小病毒感染引起的暂时性再生障碍危象中)。血清中检测到高浓度的B19细小病毒,在几例患者中,相隔数周或数月的样本中均有发现。在3例研究患者的骨髓中存在病毒DNA和衣壳蛋白,通过Southern分析检测到活跃的病毒复制。捕获免疫测定中无抗病毒IgG,抗病毒IgM无或水平极低。患者没有传染性红斑的症状,而在免疫功能正常的人中,这种病毒会引发该疾病。6例患者接受了静脉注射商用免疫球蛋白治疗方案。在所有病例中,这种治疗导致血清病毒浓度迅速降低,红细胞生成完全恢复。DNA杂交研究预测了2例复发情况,这2例患者经再次治疗成功。
B19细小病毒是HIV感染患者严重慢性贫血的可治愈病因。识别并治疗该人群中的细小病毒将避免红细胞输血,并应防止病毒传播给其他人群,包括免疫抑制人群和育龄妇女。