Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Tissue Injury and Leukocyte Changes in Post-Acute Sequelae of SARS-CoV-2: Review of 2833 Post-acute Patient Outcomes per Immune Dysregulation and Microbial Translocation in Long COVID

Version 1 : Received: 19 October 2022 / Approved: 24 October 2022 / Online: 24 October 2022 (02:12:06 CEST)

A peer-reviewed article of this Preprint also exists.

Islam Md. S., Wang Z, Abdel-Mohsen M., Chen X., Montaner L.J. Tissue injury and leukocyte changes in post-acute sequelae of SARS-CoV-2: review of 2833 post-acute patient outcomes per immune dysregulation and microbial translocation in long COVID. Journal of Leukocyte Biology, doi.org/10.1093/jleuko/qiac001, 113 (3), 2023 Islam Md. S., Wang Z, Abdel-Mohsen M., Chen X., Montaner L.J. Tissue injury and leukocyte changes in post-acute sequelae of SARS-CoV-2: review of 2833 post-acute patient outcomes per immune dysregulation and microbial translocation in long COVID. Journal of Leukocyte Biology, doi.org/10.1093/jleuko/qiac001, 113 (3), 2023

Abstract

A significant number of persons with coronavirus disease 2019 (COVID-19) experience persistent, recurrent, or new symptoms several months after the acute stage of severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) infection. This phenomenon, termed Post-Acute Sequelae of SARS-CoV-2 (PASC) or Long COVID, is associated with high viral titers during acute infection, a persistently hyperactivated immune system, tissue injury by NETosis-induced micro-thrombofibrosis (NETinjury), microbial translocation, complement deposition, fibrotic macrophages, the presence of auto-antibodies, and lymphopenic immune environments. Here, we review the current literature on the immunological imbalances that occur during PASC. Specifically, we focus on data supporting common immunopathogenesis and tissue injury mechanisms shared across this highly heterogenous disorder including NETosis, coagulopathy, and fibrosis. Mechanisms include changes in leukocyte subsets/functions, fibroblast activation, cytokine imbalances, lower cortisol, autoantibodies, co-pathogen reactivation, and residual immune activation driven by persistent viral antigens and/or microbial translocation. Taken together, we develop the premise that SARS-CoV-2 infection results in PASC as a consequence of acute and/or persistent single or multiple organ injury mediated by PASC determinants to include degree of host response (inflammation, NETinjury), residual viral antigen (persistent antigen) and exogenous factors (microbial translocation). Determinants of PASC may be amplified by co-morbidities, age, and sex. Keywords: long COVID, PASC, long haulers, NETosis, T cell, NK cell, DC, neutrophil,

Keywords

long COVID; PASC; long haulers; NETosis; T cell; NK cell; DC; neutrophil; macrophage

Subject

Biology and Life Sciences, Virology

Comments (0)

We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.

Leave a public comment
Send a private comment to the author(s)
* All users must log in before leaving a comment
Views 0
Downloads 0
Comments 0
Metrics 0


×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.
We use cookies on our website to ensure you get the best experience.
Read more about our cookies here.