Citation Information: JCI Insight. 2023;8(11):e169515. https://doi.org/10.1172/jci.insight.169515.
Abstract
Some individuals do not return to baseline health following SARS-CoV-2 infection, leading to a condition known as long COVID. The underlying pathophysiology of long COVID remains unknown. Given that autoantibodies have been found to play a role in severity of SARS-CoV-2 infection and certain other post-COVID sequelae, their potential role in long COVID is important to investigate. Here, we apply a well-established, unbiased, proteome-wide autoantibody detection technology (T7 phage-display assay with immunoprecipitation and next-generation sequencing, PhIP-Seq) to a robustly phenotyped cohort of 121 individuals with long COVID, 64 individuals with prior COVID-19 who reported full recovery, and 57 pre-COVID controls. While a distinct autoreactive signature was detected that separated individuals with prior SARS-CoV-2 infection from those never exposed to SARS-CoV-2, we did not detect patterns of autoreactivity that separated individuals with long COVID from individuals fully recovered from COVID-19. These data suggest that there are robust alterations in autoreactive antibody profiles due to infection; however, no association of autoreactive antibodies and long COVID was apparent by this assay.
Authors
Aaron Bodansky, Chung-Yu Wang, Aditi Saxena, Anthea Mitchell, Andrew F. Kung, Saki Takahashi, Khamal Anglin, Beatrice Huang, Rebecca Hoh, Scott Lu, Sarah A. Goldberg, Justin Romero, Brandon Tran, Raushun Kirtikar, Halle Grebe, Matthew So, Bryan Greenhouse, Matthew S. Durstenfeld, Priscilla Y. Hsue, Joanna Hellmuth, J. Daniel Kelly, Jeffrey N. Martin, Mark S. Anderson, Steven G. Deeks, Timothy J. Henrich, Joseph L. DeRisi, Michael J. Peluso
