Serotherapy treats a transplant hurdle Cytomegalovirus (CMV) infection and reactivation are common and potentially fatal complications after bone marrow or hematopoietic stem cell transplantation (BMT). Martins et al. developed faithful preclinical murine models of CMV reactivation following BMT and found that humoral immunity can prevent this process (see the Perspective by Alegre). After BMT, antiviral antibodies that would have kept CMV at bay dwindle because host plasma cells are ablated and the donor B cell pool reconstitutes poorly. CMV reactivation was prevented by transferring antibody-containing immune serum. Such a therapeutic strategy would avoid some limitations of cellular therapies for BMT patients. Science, this issue p. 288; see also p. 232 Transfer of strain-specific antibodies after bone marrow transplant prevents cytomelagovirus reactivation in the recipient. Cytomegalovirus infection is a frequent and life-threatening complication that significantly limits positive transplantation outcomes. We developed preclinical mouse models of cytomegalovirus reactivation after transplantation and found that humoral immunity is essential for preventing viral recrudescence. Preexisting antiviral antibodies decreased after transplant in the presence of graft-versus-host disease and were not replaced, owing to poor reconstitution of donor B cells and elimination of recipient plasma cells. Viral reactivation was prevented by the transfer of immune serum, without a need to identify and target specific antigenic determinants. Notably, serotherapy afforded complete protection, provided that the serum was matched to the infecting viral strain. Thus, we define the mechanisms for cytomegalovirus reactivation after transplantation and identify a readily translatable strategy of exceptional potency, which avoids the constraints of cellular therapies.

中文翻译：

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菌株特异性抗体疗法可防止移植后巨细胞病毒再激活

血清疗法治疗移植障碍 巨细胞病毒 (CMV) 感染和再激活是骨髓或造血干细胞移植 (BMT) 后常见且可能致命的并发症。马丁斯等人。开发了 BMT 后 CMV 再激活的可靠的临床前小鼠模型，并发现体液免疫可以阻止这一过程（参见 Alegre 的观点）。在 BMT 之后，由于宿主浆细胞被消融并且供体 B 细胞库重建不佳，本应阻止 CMV 产生的抗病毒抗体会减少。通过转移含有抗体的免疫血清来防止 CMV 再激活。这种治疗策略将避免 BMT 患者细胞疗法的一些局限性。科学，这个问题 p。288; 另见第。232 骨髓移植后菌株特异性抗体的转移可防止接受者体内的巨细胞病毒再激活。巨细胞病毒感染是一种常见且危及生命的并发症，严重限制了阳性移植结果。我们开发了移植后巨细胞病毒再激活的临床前小鼠模型，发现体液免疫对于防止病毒复发至关重要。由于供体 B 细胞的重建不良和受体浆细胞的清除，在移植后存在移植物抗宿主病的情况下，预先存在的抗病毒抗体减少，并且没有被替换。免疫血清的转移可防止病毒再激活，而无需识别和靶向特定的抗原决定簇。值得注意的是，血清疗法提供了完全的保护，前提是血清与感染病毒株相匹配。因此，我们定义了移植后巨细胞病毒再激活的机制，并确定了一种具有特殊效力的易于翻译的策略，从而避免了细胞疗法的限制。