Kupfer Bernd, Ruf Torsten, Matz Bertfried, Nattermann Jacob, Spengler Ulrich, Rockstroh Jürgen K, Brackmann Hans H, Blümel Johannes, Tacke Michael, Kaiser Rolf
Institute of Medical Microbiology and Immunology, University of Bonn, Sigmund Freud Str. 25, D-53105 Bonn, Germany.
J Clin Virol. 2005 Sep;34(1):42-7. doi: 10.1016/j.jcv.2005.01.008.
Until the mandatory introduction of viral inactivation techniques of blood plasma products in the early 1980s many recipients of these products were infected with various viral pathogens.
To determine the rate of transmission of GB virus C/hepatitis G virus (GBV-C/HGV) HCV, and HIV through non-virus-inactivated clotting factor concentrates in hemophiliacs, as well as the relation between amount of administered clotting factor and risk for GBV-C/HGV infection.
In this cross-sectional study, we determined retrospectively the rates of infection markers for GBV-C/HGV, HCV, and HIV in a German cohort of hemophiliacs treated with documented amounts of non-virus-inactivated clotting factor concentrates (group A) and in a second group of hemophiliacs who were treated exclusively with virus-inactivated clotting factor (group B). The presence of anti-virus antibodies was determined by ELISA. Viral RNA was detected by RT-PCR. Markers for viral infections were compared to amounts of administered non-virus-inactivated clotting factor.
Among hemophiliacs treated with documented amounts of non-virus-inactivated clotting factor the prevalence for GBV-C/HGV, HCV, and HIV was 40.3%, 98.6%, and 56.3%, respectively. In contrast to HIV, the rate of GBV-C/HGV infections did not increase with increasing amounts of consumed non-inactivated clotting factor. Even in the subgroup of heavily treated hemophiliacs the rate of GBV-C/HGV infection markers did not exceed 45%.
The amount of non-virus-inactivated clotting factor is not predictive for the risk of GBV-C/HGV infection in hemophiliacs. Despite repeated parenteral exposure more than 55% of hemophiliacs were not infected with GBV-C/HGV. Our findings indicate a high frequency of host factors preventing parenteral transmission of GBV-C/HGV.
直到20世纪80年代初强制引入血浆制品病毒灭活技术之前,许多这些制品的接受者感染了各种病毒病原体。
确定GB病毒C/庚型肝炎病毒(GBV-C/HGV)、丙型肝炎病毒(HCV)和人类免疫缺陷病毒(HIV)通过未进行病毒灭活的凝血因子浓缩物在血友病患者中的传播率,以及所输注凝血因子的量与GBV-C/HGV感染风险之间的关系。
在这项横断面研究中,我们回顾性地确定了德国一组接受过记录用量的未进行病毒灭活的凝血因子浓缩物治疗的血友病患者(A组)以及另一组仅接受过病毒灭活凝血因子治疗的血友病患者(B组)中GBV-C/HGV、HCV和HIV感染标志物的发生率。通过酶联免疫吸附测定(ELISA)确定抗病毒抗体的存在。通过逆转录聚合酶链反应(RT-PCR)检测病毒RNA。将病毒感染标志物与所输注的未进行病毒灭活的凝血因子的量进行比较。
在接受过记录用量的未进行病毒灭活的凝血因子治疗的血友病患者中,GBV-C/HGV、HCV和HIV的患病率分别为40.3%、98.6%和56.3%。与HIV不同,GBV-C/HGV感染率并未随着未灭活凝血因子消耗量的增加而升高。即使在接受大量治疗的血友病患者亚组中,GBV-C/HGV感染标志物的发生率也未超过45%。
未进行病毒灭活的凝血因子的量不能预测血友病患者感染GBV-C/HGV的风险。尽管反复经肠道外接触,超过55%的血友病患者未感染GBV-C/HGV。我们的研究结果表明存在高频率的宿主因素可阻止GBV-C/HGV经肠道外传播。