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首页> 外文期刊>Antimicrobial agents and chemotherapy. >Recovery of humoral immunity is critical for successful antiviral therapy in disseminated mouse adenovirus type 1 infection.
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Recovery of humoral immunity is critical for successful antiviral therapy in disseminated mouse adenovirus type 1 infection.

机译：体液免疫力的恢复对于弥散性1型小鼠腺病毒感染成功进行抗病毒治疗至关重要。

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Severe adenovirus infections in transplant recipients undergoing immunosuppressive therapy are of increasing concern. Controversy exists on the contribution of antiviral therapy and the host immune response to recovery from these infections. Here, we established a systemic mouse adenovirus type 1 (MAV-1) infection in cyclophosphamide (CyP)-treated BALB/c mice. CyP was administered at 100 mg per kg of body weight every other day for 2, 3, or 4 weeks, thereby inducing general but reversible leukopenia, with a major suppression of the B-cell numbers and functionality that was more pronounced than that seen with T cells. The outcome of MAV-1 infection was dependent on the duration of CyP therapy, as the mice with the most severe immunosuppression were the most vulnerable to MAV-1-induced hemorrhagic enteritis and mortality. The protective effect of concomitant antiviral therapy with cidofovir depended on the level of immunosuppression. The combination of cidofovir treatment with the withdrawal of immunosuppression was the most successful regimen for increasing survival rates. Survival was clearly correlated with the clearance of virus and increased titers of MAV-1-specific antibodies in sera. In addition, the passive transfer of MAV-1-specific immunoglobulin G into MAV-1-infected SCID BALB/c mice caused a marked delay in mortality, the extent of the delay being dependent on the titer of MAV-1-specific antibodies. Based on the critical role of the humoral immune response in the early defense against disseminated adenovirus infection, the concomitant use of adenovirus-specific immunoglobulins and antiviral therapy should be considered for transplant patients at risk for severe adenovirus infections.
机译：接受免疫抑制治疗的移植受体中的严重腺病毒感染日益引起人们的关注。关于抗病毒治疗的贡献以及宿主对从这些感染中恢复的免疫反应存在争议。在这里，我们在环磷酰胺（CyP）处理的BALB / c小鼠中建立了系统性小鼠1型腺病毒（MAV-1）感染。 CyP每隔2、3或4周每公斤体重以100 mg的剂量给药，从而诱发一般性但可逆的白细胞减少症，对B细胞数量和功能的主要抑制作用比对于观察到的更为明显。 T细胞。 MAV-1感染的结果取决于CyP治疗的持续时间，因为免疫抑制最严重的小鼠最容易受到MAV-1诱导的出血性肠炎和死亡率的影响。西多福韦同时抗病毒治疗的保护作用取决于免疫抑制水平。西多福韦治疗与取消免疫抑制相结合是提高生存率的最成功方案。存活率与病毒清除率和血清中MAV-1特异性抗体滴度增加明显相关。此外，MAV-1特异性免疫球蛋白G被动转移到感染了MAV-1的SCID BALB / c小鼠中，导致死亡率显着延迟，延迟的程度取决于MAV-1特异性抗体的效价。基于体液免疫反应在早期预防弥漫性腺病毒感染中的关键作用，对于有严重腺病毒感染风险的移植患者，应考虑同时使用腺病毒特异性免疫球蛋白和抗病毒治疗。

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