Prolonged severe acute respiratory syndrome coronavirus 2 persistence, attenuated immunologic response, and viral evolution in a solid organ transplant patient.

Prolonged severe acute respiratory syndrome coronavirus 2 persistence, attenuated immunologic response, and viral evolution in a solid organ transplant patient.
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DOI:
10.1111/ajt.16837
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发表时间:
2022-03
期刊:
American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
影响因子:
--
通讯作者:
Yin MT
Yin MT
中科院分区:
其他
文献类型:
--
作者:
Purpura LJ;Chang M;Annavajhala MK;Mohri H;Liu L;Shah J;Cantos A;Medrano N;Laracy J;Scully B;Miko BA;Habal M;Pereira MR;Tsuji M;Ho DD;Uhlemann AC;Yin MT

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与免疫功能正常的宿主不同,免疫抑制患者感染严重急性呼吸综合征冠状病毒2后病毒持续存在的时间可以延长。在这里,我们提出了一个案件的病毒持续超过19周的病人与历史的实体器官移植,并探讨临床,病毒学和免疫过程。我们的患者在138天时仍然表现出病毒持续存在,聚合酶链反应循环阈值较低,并且有证据表明病毒序列持续进化,表明病毒正在复制。这些发现对免疫抑制患者的感染预防和控制建议具有重要意义。免疫应答,包括中和抗体滴度、T细胞活性和细胞因子水平,在诊断后约44-72天达到峰值。抗S三聚体抗体在所有时间点均较低,并且T细胞应答在第119天减弱。随着免疫反应减弱和病毒载量增加,出现了遗传多样性增加,这表明了病毒变体发展的机制。
Unlike immunocompetent hosts, the duration of viral persistence after infection with severe acute respiratory syndrome coronavirus 2 can be prolonged in immunosuppressed patients. Here, we present a case of viral persistence for over 19 weeks in a patient with a history of solid organ transplant and explore the clinical, virologic, and immunologic course. Our patient still demonstrated viral persistence at 138 days with low polymerase chain reaction cycle threshold values and evidence of continuing viral sequence evolution indicative of ongoing virus replication. These findings have important implications for infection prevention and control recommendations in immunosuppressed patients. Immune response, including neutralizing antibody titers, T cell activity, and cytokine levels, peaked around days 44–72 after diagnosis. Anti-S trimer antibodies were low at all time points, and T cell response was attenuated by day 119. As immune response waned and viral load increased, increased genetic diversity emerged, suggesting a mechanism for the development of viral variants.
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