Long-term SARS-CoV-2-specific immune and inflammatory responses in individuals recovering from COVID-19 with and without post-acute symptoms

COVID-19 康复者(无论是否出现急性后期症状)的长期 SARS-CoV-2 特异性免疫和炎症反应

阅读:3
作者:Michael J Peluso ,Amelia N Deitchman ,Leonel Torres ,Nikita S Iyer ,Sadie E Munter ,Christopher C Nixon ,Joanna Donatelli ,Cassandra Thanh ,Saki Takahashi ,Jill Hakim ,Keirstinne Turcios ,Owen Janson ,Rebecca Hoh ,Viva Tai ,Yanel Hernandez ,Emily A Fehrman ,Matthew A Spinelli ,Monica Gandhi ,Lan Trinh ,Terri Wrin ,Christos J Petropoulos ,Francesca T Aweeka ,Isabel Rodriguez-Barraquer ,J Daniel Kelly ,Jeffrey N Martin ,Steven G Deeks ,Bryan Greenhouse ,Rachel L Rutishauser ,Timothy J Henrich

Abstract

We describe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-specific T cell responses, soluble markers of inflammation, and antibody levels and neutralization capacity longitudinally in 70 individuals with PCR-confirmed SARS-CoV-2 infection. Participants represent a spectrum of illness and recovery, including some with persistent viral shedding in saliva and many experiencing post-acute sequelae of SARS-CoV-2 infection (PASC). T cell responses remain stable for up to 9 months. Whereas the magnitude of early CD4+ T cell immune responses correlates with severity of initial infection, pre-existing lung disease is independently associated with higher long-term SARS-CoV-2-specific CD8+ T cell responses. Among participants with PASC 4 months following coronavirus disease 2019 (COVID-19) symptom onset, we observe a lower frequency of CD8+ T cells expressing CD107a, a marker of degranulation, in response to Nucleocapsid (N) peptide pool stimulation, and a more rapid decline in the frequency of N-specific interferon-γ-producing CD8+ T cells. Neutralizing antibody levels strongly correlate with SARS-CoV-2-specific CD4+ T cell responses.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。