- Bodansky, Aaron;
- Wang, Chung-Yu;
- Saxena, Aditi;
- Mitchell, Anthea;
- Kung, Andrew;
- Takahashi, Saki;
- Anglin, Khamal;
- Hoh, Rebecca;
- Lu, Scott;
- Goldberg, Sarah;
- Romero, Justin;
- Tran, Brandon;
- Kirtikar, Raushun;
- Grebe, Halle;
- So, Matthew;
- Hsue, Priscilla;
- Hellmuth, Joanna;
- Kelly, J;
- Henrich, Timothy;
- Greenhouse, Bryan;
- Martin, Jeffrey;
- Anderson, Mark;
- Deeks, Steven;
- Derisi, Joseph;
- Peluso, Michael;
- Durstenfeld, Matthew;
- Huang, Beatrice
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.